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Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 October 2021) | Viewed by 97524

Special Issue Editors

Dr. Antonella Fioravanti

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Guest Editor
1. Retired from Rheumatology Unit of Azienda Ospedaliera Senese, Siena, Italy
2. Center of Biotechnology, Sbarro Institute for Cancer Research and Molecular Medicine, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
3. President of OMTh, Levico Terme, Italy
Interests: osteoarthritis; rheumatic diseases; microRNA; chondrocyte cultures; psoriatic arthritis; rheumatoid arthritis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Francesco Dotta

E-Mail Website
Guest Editor
Diabetes Unit, Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Antonio Giordano

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Guest Editor
1. Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
2. Department of Medical Biotechnologies, University of Siena, Siena, Italy
Interests: cell cycle; tumor suppressor genes; RB family; CDK inhibitors; environment and cancer
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Luigi Pirtoli

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Guest Editor
1. Department of Biology, College of Science and Technology, Temple University, Philadelphia, PA, USA
2. Radiation Oncology Unit, Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy (Retired)
Interests: oncology; radiobiology; radiotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

MicroRNAs (miRNAs)—small noncoding RNAs 19–24 nucleotides long—have emerged as important post-transcriptional regulators of gene expression, by binding specific sequences within target messenger RNA (mRNA). The importance of epigenetic miRNA regulation in cellular function is becoming increasingly clear as novel targets are discovered. These targets have been associated with controlling important cellular processes, such as lipid metabolism, apoptosis, differentiation, and organ development. Importantly, miRNAs have recently been addressed as novel mediators of cell–cell communication, being secreted from cells, and are found in many different biological fluids. Such characteristics also make miRNA potential disease biomarkers.

Alterations in miRNA expression have been linked to pathological features, such as inflammatory, degenerative, or autoimmune processes, and are involved in several disease outcomes, including cancer, cardiovascular diseases, diabetes mellitus, and rheumatic and neurological disorders.

Despite these processes having been extensively studied, their detailed mechanisms are not yet fully understood.

Reactive oxygen species (ROS) are free radicals containing oxygen molecules derived from cellular oxidative metabolism, including enzyme activities and mitochondrial respiration, and which play a pivotal role in many cellular functions. Whereas ROS are essential for normal cellular processes, the aberrant production of ROS or the failure of the capacity to scavenge excessive ROS determines an altered redox status with an excessive synthesis of free radicals, leading to an imbalance in the redox environment of the cell.

The loss of normal ROS levels can result in damage to lipids, proteins, and DNA, all of which contribute to the development of various pathologies such as neurological disorders, rheumatic and cardiovascular diseases, diabetes, and cancer.

Recent research highlights conditions where there is crosstalk between miRNA and oxidative stress, even if this complex and mutual interaction needs further elucidation.

In this regard, we invite investigators to contribute original research articles and review articles that will stimulate the continuing efforts to understand the mechanisms underlying the interaction between miRNA and oxidative stress under normal and diseased processes, toward developing strategies to treat these pathological conditions as well as to identify novel biomarkers of disease.

Dr. Antonella Fioravanti
Prof. Dr. Francesco Dotta
Prof. Dr. Antonio Giordano
Prof. Dr. Luigi Pirtoli
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • microRNA
  • oxidative stress
  • cardiovascular diseases
  • rheumatic diseases
  • cancer
  • diabetes
  • neurological disorders
  • multiple sclerosis

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Published Papers (22 papers)

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Editorial

Jump to: Research, Review

6 pages, 214 KiB  
Editorial
Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0
by Antonella Fioravanti, Antonio Giordano, Francesco Dotta and Luigi Pirtoli
Int. J. Mol. Sci. 2022, 23(12), 6831; https://doi.org/10.3390/ijms23126831 - 20 Jun 2022
Cited by 6 | Viewed by 2791
Abstract
MicroRNAs (miRNAs) are a class of small non-coding RNAs around 22 nucleotides long that regulate gene expression by binding specific sequences within target messenger RNA (mRNA) [...] Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)

Research

Jump to: Editorial, Review

14 pages, 4070 KiB  
Article
Putative Circulating MicroRNAs Are Able to Identify Patients with Mitral Valve Prolapse and Severe Regurgitation
by Paola Songia, Mattia Chiesa, Valentina Alfieri, Ilaria Massaiu, Donato Moschetta, Veronika Myasoedova, Vincenza Valerio, Laura Fusini, Paola Gripari, Marco Zanobini and Paolo Poggio
Int. J. Mol. Sci. 2021, 22(4), 2102; https://doi.org/10.3390/ijms22042102 - 20 Feb 2021
Cited by 7 | Viewed by 1893
Abstract
Mitral valve prolapse (MVP) associated with severe mitral regurgitation is a debilitating disease with no pharmacological therapies available. MicroRNAs (miRNA) represent an emerging class of circulating biomarkers that have never been evaluated in MVP human plasma. Our aim was to identify a possible [...] Read more.
Mitral valve prolapse (MVP) associated with severe mitral regurgitation is a debilitating disease with no pharmacological therapies available. MicroRNAs (miRNA) represent an emerging class of circulating biomarkers that have never been evaluated in MVP human plasma. Our aim was to identify a possible miRNA signature that is able to discriminate MVP patients from healthy subjects (CTRL) and to shed light on the putative altered molecular pathways in MVP. We evaluated a plasma miRNA profile using Human MicroRNA Card A followed by real-time PCR validations. In addition, to assess the discriminative power of selected miRNAs, we implemented a machine learning analysis. MiRNA profiling and validations revealed that miR-140-3p, 150-5p, 210-3p, 451a, and 487a-3p were significantly upregulated in MVP, while miR-223-3p, 323a-3p, 340-5p, and 361-5p were significantly downregulated in MVP compared to CTRL (p ≤ 0.01). Functional analysis identified several biological processes possible linked to MVP. In addition, machine learning analysis correctly classified MVP patients from CTRL with high accuracy (0.93) and an area under the receiving operator characteristic curve (AUC) of 0.97. To the best of our knowledge, this is the first study performed on human plasma, showing a strong association between miRNAs and MVP. Thus, a circulating molecular signature could be used as a first-line, fast, and cheap screening tool for MVP identification. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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19 pages, 4683 KiB  
Article
MiR-302 Regulates Glycolysis to Control Cell-Cycle during Neural Tube Closure
by Rachel A. Keuls, Karin Kojima, Brittney Lozzi, John W. Steele, Qiuying Chen, Steven S. Gross, Richard H. Finnell and Ronald J. Parchem
Int. J. Mol. Sci. 2020, 21(20), 7534; https://doi.org/10.3390/ijms21207534 - 13 Oct 2020
Cited by 17 | Viewed by 4289
Abstract
Neural tube closure is a critical early step in central nervous system development that requires precise control of metabolism to ensure proper cellular proliferation and differentiation. Dysregulation of glucose metabolism during pregnancy has been associated with neural tube closure defects (NTDs) in humans [...] Read more.
Neural tube closure is a critical early step in central nervous system development that requires precise control of metabolism to ensure proper cellular proliferation and differentiation. Dysregulation of glucose metabolism during pregnancy has been associated with neural tube closure defects (NTDs) in humans suggesting that the developing neuroepithelium is particularly sensitive to metabolic changes. However, it remains unclear how metabolic pathways are regulated during neurulation. Here, we used single-cell mRNA-sequencing to analyze expression of genes involved in metabolism of carbon, fats, vitamins, and antioxidants during neurulation in mice and identify a coupling of glycolysis and cellular proliferation to ensure proper neural tube closure. Using loss of miR-302 as a genetic model of cranial NTD, we identify misregulated metabolic pathways and find a significant upregulation of glycolysis genes in embryos with NTD. These findings were validated using mass spectrometry-based metabolite profiling, which identified increased glycolytic and decreased lipid metabolites, consistent with a rewiring of central carbon traffic following loss of miR-302. Predicted miR-302 targets Pfkp, Pfkfb3, and Hk1 are significantly upregulated upon NTD resulting in increased glycolytic flux, a shortened cell cycle, and increased proliferation. Our findings establish a critical role for miR-302 in coordinating the metabolic landscape of neural tube closure. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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17 pages, 2603 KiB  
Article
Extracellular Vesicles Mediate Anti-Oxidative Response—In Vitro Study in the Ocular Drainage System
by Natalie Lerner, Itay Chen, Sofia Schreiber-Avissar and Elie Beit-Yannai
Int. J. Mol. Sci. 2020, 21(17), 6105; https://doi.org/10.3390/ijms21176105 - 25 Aug 2020
Cited by 25 | Viewed by 2712
Abstract
The importance of extracellular vesicles (EVs) as signaling mediators has been emphasized for several pathways with only limited data regarding their role as protective messages during oxidative stress (OS). The ocular drainage system is unique by being continuously exposed to OS and having [...] Read more.
The importance of extracellular vesicles (EVs) as signaling mediators has been emphasized for several pathways with only limited data regarding their role as protective messages during oxidative stress (OS). The ocular drainage system is unique by being continuously exposed to OS and having a one-way flow of the aqueous humor carrying EVs taking role in glaucoma disease. Here, we aimed to examine the ability of EVs derived from the non-pigmented ciliary epithelium (NPCE)—the aqueous humor producing cells exposed to OS—to deliver protecting messages to the trabecular meshwork (TM)—the aqueous humor draining cells—a process with significance to the pathophysiology of glaucoma disease. EVs extracted from media of NPCE cells exposed to non-lethal OS and their unstressed control were incubated with TM cells. The effects of EVs derived from oxidative stressed cells on the activation of the nuclear factor erythroid 2-related factor 2-Kelch-like ECH-associated protein 1 (Nrf2-Keap1), a major OS pathway, and of the Wnt pathway, known for its role in primary open-angle glaucoma, were evaluated. EVs derived from oxidized NPCE cells significantly protected TM cells from direct OS. The TM cells uptake of EVs from oxidized NPCE and their cytosolic Nrf2 levels were significantly higher at 8 h post-exposure. EVs derived from oxidized NPCE cells significantly attenuated Wnt protein expression in TM cells and activated major antioxidant genes as measured by qRT-PCR. TM cells exposed to EVs derived from oxidized NPCE cells exhibited significantly lower OS and higher super oxide dismutase and catalase activity. Finally, we were able to show that carbonylated proteins and products of oxidized protein are presented in significantly higher levels in EVs derived from oxidized NPCE cells, supporting their suggested role in the signaling process. We hypothesize that these findings may have implications beyond understanding the pathophysiology of glaucoma disease and that transmitting signals that activate the antioxidant system in target cells represent a broad response common to many tissues communication. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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14 pages, 2064 KiB  
Article
Identification of circRNA-Associated-ceRNA Networks Involved in Milk Fat Metabolism under Heat Stress
by Dongyang Wang, Zujing Chen, Xiaona Zhuang, Junyi Luo, Ting Chen, Qianyun Xi, Yongliang Zhang and Jiajie Sun
Int. J. Mol. Sci. 2020, 21(11), 4162; https://doi.org/10.3390/ijms21114162 - 11 Jun 2020
Cited by 32 | Viewed by 3477
Abstract
Summer temperatures are generally high in Southern China, and cows are likely to suffer a heat stress reaction. Heat stress will have a negative impact on the performance of dairy cows; however, the mechanism by which high temperature affects lactation is not clear. [...] Read more.
Summer temperatures are generally high in Southern China, and cows are likely to suffer a heat stress reaction. Heat stress will have a negative impact on the performance of dairy cows; however, the mechanism by which high temperature affects lactation is not clear. CircRNA is a type of non-coding RNA discovered in recent years, which performs a crucial function in many biological activities. However, the effects of circRNA on lactation function of dairy cows under heat stress is unknown. The present study aimed to explore the expression levels of circRNA in the mammary gland tissue of cows under heat stress. Firstly, we collected blood and milk samples of summer and winter cows and evaluated lactation performance using serum indicators, milk production, and milk composition. Incorporating the calculation of the temperature and humidity index, we conformed the heat stress status of cows in summer. Heat stress increased the concentration of HSP70 and decreased the concentration of SOD and PRL. Heat stress not only reduced milk yield but also affected milk quality, with milk lactose and milk protein decreasing with increased temperature. The analysis of the fatty acid composition in summer milk found significantly reduced concentrations of unsaturated fatty acids, especially long-chain unsaturated fatty acids. Sequencing of the cow’s mammary gland transcriptome revealed that compared to the appropriate temperature (ST) group, the heat stress (HS) group had a total of 2204 upregulated and 3501 downregulated transcripts. GO enrichment and KEGG pathway analysis showed that these genes were mainly related to milk fat metabolism. In addition, 19 upregulated and 19 downregulated circRNA candidates were found in response to heat stress. We used Pearson’s test to establish the correlation of circRNA-mRNA and identified four pairs of circRNA-miRNA networks between four circRNAs, six miRNAs, and the CD36 gene. In this study, we revealed the possible role of circRNAs in lactation of dairy cows and identified that circRNA-miRNA-mRNA networks might exist in the cow’s mammary glands, providing valuable experience for dairy lactation and milk quality. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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23 pages, 5082 KiB  
Article
Hydrostatic Pressure Regulates Oxidative Stress through microRNA in Human Osteoarthritic Chondrocytes
by Sara Cheleschi, Marcella Barbarino, Ines Gallo, Sara Tenti, Maria Bottaro, Elena Frati, Stefano Giannotti and Antonella Fioravanti
Int. J. Mol. Sci. 2020, 21(10), 3653; https://doi.org/10.3390/ijms21103653 - 21 May 2020
Cited by 19 | Viewed by 3464
Abstract
Hydrostatic pressure (HP) modulates chondrocytes metabolism, however, its ability to regulate oxidative stress and microRNAs (miRNA) has not been clarified. The aim of this study was to investigate the role of miR-34a, miR-146a, and miR-181a as possible mediators of HP effects on oxidative [...] Read more.
Hydrostatic pressure (HP) modulates chondrocytes metabolism, however, its ability to regulate oxidative stress and microRNAs (miRNA) has not been clarified. The aim of this study was to investigate the role of miR-34a, miR-146a, and miR-181a as possible mediators of HP effects on oxidative stress in human osteoarthritis (OA) chondrocytes. Chondrocytes were exposed to cyclic low HP (1–5 MPa) and continuous static HP (10 MPa) for 3~h. Metalloproteinases (MMPs), disintegrin and metalloproteinase with thrombospondin motif (ADAMTS)-5, type II collagen (Col2a1), miR-34a, miR-146a, miR-181a, antioxidant enzymes, and B-cell lymphoma 2 (BCL2) were evaluated by quantitative real-time polymerase chain reaction qRT-PCR, apoptosis and reactive oxygen species ROS production by cytometry, and β-catenin by immunofluorescence. The relationship among HP, the studied miRNA, and oxidative stress was assessed by transfection with miRNA specific inhibitors. Low cyclical HP significantly reduced apoptosis, the gene expression of MMP-13, ADAMTS5, miRNA, the production of superoxide anion, and mRNA levels of antioxidant enzymes. Conversely, an increased Col2a1 and BCL2 genes was observed. β-catenin protein expression was reduced in cells exposed to HP 1–5 MPa. Opposite results were obtained following continuous static HP application. Finally, miRNA silencing enhanced low HP and suppressed continuous HP-induced effects. Our data suggest miRNA as one of the mechanisms by which HP regulates chondrocyte metabolism and oxidative stress, via Wnt/β-catenin pathway. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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18 pages, 1780 KiB  
Article
A Circulating MicroRNA Profile in a Laser-Induced Mouse Model of Choroidal Neovascularization
by Christina Kiel, Patricia Berber, Marcus Karlstetter, Alexander Aslanidis, Tobias Strunz, Thomas Langmann, Felix Grassmann and Bernhard H.F. Weber
Int. J. Mol. Sci. 2020, 21(8), 2689; https://doi.org/10.3390/ijms21082689 - 13 Apr 2020
Cited by 8 | Viewed by 3201
Abstract
Choroidal neovascularization (CNV) is a pathological process in which aberrant blood vessels invade the subretinal space of the mammalian eye. It is a characteristic feature of the prevalent neovascular age-related macular degeneration (nAMD). Circulating microRNAs (cmiRNAs) are regarded as potentially valuable biomarkers for [...] Read more.
Choroidal neovascularization (CNV) is a pathological process in which aberrant blood vessels invade the subretinal space of the mammalian eye. It is a characteristic feature of the prevalent neovascular age-related macular degeneration (nAMD). Circulating microRNAs (cmiRNAs) are regarded as potentially valuable biomarkers for various age-related diseases, including nAMD. Here, we investigated cmiRNA expression in an established laser-induced CNV mouse model. Upon CNV induction in C57Bl/6 mice, blood-derived cmiRNAs were initially determined globally by RNA next generation sequencing, and the most strongly dysregulated cmiRNAs were independently replicated by quantitative reverse transcription PCR (RT-qPCR) in blood, retinal, and retinal pigment epithelium (RPE)/choroidal tissue. Our findings suggest that two miRNAs, mmu-mir-486a-5p and mmur-mir-92a-3p, are consistently dysregulated during CNV formation. Furthermore, in functional in vitro assays, a significant impact of mmu-mir-486a-5p and mmu-mir-92a-3p on murine microglial cell viability was observed, while mmu-mir-92a-3p also showed an impact on microglial mobility. Taken together, we report a robust dysregulation of two miRNAs in blood and RPE/choroid after laser-induced initiation of CNV lesions in mice, highlighting their potential role in pathology and eventual therapy of CNV-associated complications. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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12 pages, 1473 KiB  
Article
Exosomal MicroRNAs Released by Activated Astrocytes as Potential Neuroinflammatory Biomarkers
by Manoshi Gayen, Manish Bhomia, Nagaraja Balakathiresan and Barbara Knollmann-Ritschel
Int. J. Mol. Sci. 2020, 21(7), 2312; https://doi.org/10.3390/ijms21072312 - 27 Mar 2020
Cited by 50 | Viewed by 4863
Abstract
Neuroinflammation is a hallmark of several neurodegenerative diseases and disorders, including traumatic brain injury (TBI). Neuroinflammation results in the activation of glial cells which exacerbates the neuroinflammatory process by secretion of pro-inflammatory cytokines and results in disruption of glial transmission networks. The glial [...] Read more.
Neuroinflammation is a hallmark of several neurodegenerative diseases and disorders, including traumatic brain injury (TBI). Neuroinflammation results in the activation of glial cells which exacerbates the neuroinflammatory process by secretion of pro-inflammatory cytokines and results in disruption of glial transmission networks. The glial cells, including astrocytes, play a critical role in the maintenance of homeostasis in the brain. Activated astrocytes release several factors as part of the inflammatory process including cytokines, proteins, and microRNAs (miRNAs). MiRNAs are noncoding RNA molecules involved in normal physiological processes and disease pathogenesis. MiRNAs have been implicated as important cell signaling molecules, and they are potential diagnostic biomarkers and therapeutic targets for various diseases, including neurological disorders. Exosomal miRNAs released by astrocytic response to neuroinflammation is not yet studied. In this study, primary human astrocytes were activated by IL-1β stimulation and we examined astrocytic exosomal miRNA cargo released in a neuroinflammatory stress model. Results indicate that acute neuroinflammation and oxidative stress induced by IL-1β generates the release of a specific subset of miRNAs via exosomes, which may have a potential role in regulating the inflammatory response. Additionally, these miRNAs may serve as potential biomarkers of neuroinflammation associated with neurological disorders and injuries. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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18 pages, 1547 KiB  
Article
Integrated miRNA/mRNA Counter-Expression Analysis Highlights Oxidative Stress-Related Genes CCR7 and FOXO1 as Blood Markers of Coronary Arterial Disease
by Miguel Hueso, Adrián Mallén, Ángela Casas, Jordi Guiteras, Fabrizio Sbraga, Arnau Blasco-Lucas, Núria Lloberas, Joan Torras, Josep M Cruzado and Estanislao Navarro
Int. J. Mol. Sci. 2020, 21(6), 1943; https://doi.org/10.3390/ijms21061943 - 12 Mar 2020
Cited by 12 | Viewed by 2824
Abstract
Our interest in the mechanisms of atherosclerosis progression (ATHp) has led to the recent identification of 13 miRNAs and 1285 mRNAs whose expression was altered during ATHp. Here, we deepen the functional relationship among these 13 miRNAs and genes associated to oxidative stress, [...] Read more.
Our interest in the mechanisms of atherosclerosis progression (ATHp) has led to the recent identification of 13 miRNAs and 1285 mRNAs whose expression was altered during ATHp. Here, we deepen the functional relationship among these 13 miRNAs and genes associated to oxidative stress, a crucial step in the onset and progression of vascular disease. We first compiled a list of genes associated to the response to oxidative stress (Oxstress genes) by performing a reverse Gene Ontology analysis (rGO, from the GO terms to the genes) with the GO terms GO0006979, GO1902882, GO1902883 and GO1902884, which included a total of 417 unique Oxstress genes. Next, we identified 108 putative targets of the 13 miRNAs among these unique Oxstress genes, which were validated by an integrated miRNA/mRNA counter-expression analysis with the 1285 mRNAs that yielded 14 genes, Map2k1, Mapk1, Mapk9, Dapk1, Atp2a2, Gata4, Fos, Egfr, Foxo1, Ccr7, Vkorc1l1, Rnf7, Kcnh3, and Mgat3. GO enrichment analysis and a protein–protein-interaction network analysis (PPI) identified most of the validated Oxstress transcripts as components of signaling pathways, highlighting a role for MAP signaling in ATHp. Lastly, expression of these Oxstress transcripts was measured in PBMCs from patients suffering severe coronary artery disease, a serious consequence of ATHp. This allowed the identification of FOXO1 and CCR7 as blood markers downregulated in CAD. These results are discussed in the context of the interaction of the Oxstress transcripts with the ATHp-associated miRNAs. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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22 pages, 1825 KiB  
Article
Chemotherapeutic Stress Influences Epithelial–Mesenchymal Transition and Stemness in Cancer Stem Cells of Triple-Negative Breast Cancer
by Xiao Li, Juliane Strietz, Andreas Bleilevens, Elmar Stickeler and Jochen Maurer
Int. J. Mol. Sci. 2020, 21(2), 404; https://doi.org/10.3390/ijms21020404 - 08 Jan 2020
Cited by 29 | Viewed by 3914
Abstract
Triple-negative breast cancer (TNBC) is a subtype of breast cancer characterized by the absence of estrogen and progesterone receptors (ER, PR) and lacking an overexpression of human epidermal growth factor receptor 2 (HER2). Apart from this lack of therapeutic targets, TNBC also shows [...] Read more.
Triple-negative breast cancer (TNBC) is a subtype of breast cancer characterized by the absence of estrogen and progesterone receptors (ER, PR) and lacking an overexpression of human epidermal growth factor receptor 2 (HER2). Apart from this lack of therapeutic targets, TNBC also shows an increased capacity for early metastasis and therapy resistance. Currently, many TNBC patients receive neoadjuvant chemotherapy (NACT) upon detection of the disease. With TNBC likely being driven at least in part by a cancer stem-like cell type, we wanted to evaluate the response of primary cancer stem cells (CSCs) to standard chemotherapeutics. Therefore, we set up a survival model using primary CSCs to mimic tumor cells in patients under chemotherapy. Breast cancer stem cells (BCSCs) were exposed to chemotherapeutics with a sublethal dose for six days. Surviving cells were allowed to recover in culture medium without chemotherapeutics. Surviving and recovered cells were examined in regard to proliferation, migratory capacity, sphere forming capacity, epithelial–mesenchymal transition (EMT) factor expression at the mRNA level, and cancer-related microRNA (miRNA) profile. Our results indicate that chemotherapeutic stress enhanced sphere forming capacity of BCSCs, and changed cell morphology and EMT-related gene expression at the mRNA level, whereas the migratory capacity was unaffected. Six miRNAs were identified as potential regulators in this process. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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Review

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8 pages, 1291 KiB  
Review
miRNAs in Cardiac Myxoma: New Pathologic Findings for Potential Therapeutic Opportunities
by Antonio Nenna, Francesco Loreni, Omar Giacinto, Camilla Chello, Pierluigi Nappi, Massimo Chello and Francesco Nappi
Int. J. Mol. Sci. 2022, 23(6), 3309; https://doi.org/10.3390/ijms23063309 - 18 Mar 2022
Cited by 4 | Viewed by 1950
Abstract
MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level, contributing to all major cellular processes. The importance of miRNAs in cardiac development, heart function, and valvular heart disease has been shown in recent years, and aberrant expression of miRNA has been reported in [...] Read more.
MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level, contributing to all major cellular processes. The importance of miRNAs in cardiac development, heart function, and valvular heart disease has been shown in recent years, and aberrant expression of miRNA has been reported in various malignancies, such as gastric cancer and breast cancer. Different from other fields of investigation, the role of miRNAs in cardiac tumors still remains difficult to interpret due to the scarcity publications and a lack of narrative focus on this topic. In this article, we summarize the available evidence on miRNAs and cardiac myxomas and propose new pathways for future research. miRNAs play a part in modifying the expression of cardiac transcription factors (miR-335-5p), increasing cell cycle trigger factors (miR-126-3p), interfering with ceramide synthesis (miR-320a), inducing apoptosis (miR-634 and miR-122), suppressing production of interleukins (miR-217), and reducing cell proliferation (miR-218). As such, they have complex and interconnected roles. At present, the study of the complete mechanistic control of miRNA remains a crucial issue, as proper understanding of signaling pathways is essential for the forecasting of therapeutic implications. Other types of cardiac tumors still lack adequate investigation with regard to miRNA. Further research should aim at investigating the causal relationship between different miRNAs and cell overgrowth, considering both myxoma and other histological types of cardiac tumors. We hope that this review will help in understanding this fascinating molecular approach. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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18 pages, 1164 KiB  
Review
MicroRNAs in Valvular Heart Diseases: Biological Regulators, Prognostic Markers and Therapeutical Targets
by Francesco Nappi, Adelaide Iervolino, Sanjeet Singh Avtaar Singh and Massimo Chello
Int. J. Mol. Sci. 2021, 22(22), 12132; https://doi.org/10.3390/ijms222212132 - 09 Nov 2021
Cited by 11 | Viewed by 2406
Abstract
miRNAs have recently attracted investigators’ interest as regulators of valvular diseases pathogenesis, diagnostic biomarkers, and therapeutical targets. Evidence from in-vivo and in-vitro studies demonstrated stimulatory or inhibitory roles in mitral valve prolapse development, aortic leaflet fusion, and calcification pathways, specifically osteoblastic differentiation and [...] Read more.
miRNAs have recently attracted investigators’ interest as regulators of valvular diseases pathogenesis, diagnostic biomarkers, and therapeutical targets. Evidence from in-vivo and in-vitro studies demonstrated stimulatory or inhibitory roles in mitral valve prolapse development, aortic leaflet fusion, and calcification pathways, specifically osteoblastic differentiation and transcription factors modulation. Tissue expression assessment and comparison between physiological and pathological phenotypes of different disease entities, including mitral valve prolapse and mitral chordae tendineae rupture, emerged as the best strategies to address miRNAs over or under-representation and thus, their impact on pathogeneses. In this review, we discuss the fundamental intra- and intercellular signals regulated by miRNAs leading to defects in mitral and aortic valves, congenital heart diseases, and the possible therapeutic strategies targeting them. These miRNAs inhibitors are comprised of antisense oligonucleotides and sponge vectors. The miRNA mimics, miRNA expression vectors, and small molecules are instead possible practical strategies to increase specific miRNA activity. Advantages and technical limitations of these new drugs, including instability and complex pharmacokinetics, are also presented. Novel delivery strategies, such as nanoparticles and liposomes, are described to improve knowledge on future personalized treatment directions. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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17 pages, 825 KiB  
Review
Crosstalk between MicroRNA and Oxidative Stress in Primary Open-Angle Glaucoma
by Saray Tabak, Sofia Schreiber-Avissar and Elie Beit-Yannai
Int. J. Mol. Sci. 2021, 22(5), 2421; https://doi.org/10.3390/ijms22052421 - 28 Feb 2021
Cited by 34 | Viewed by 4028
Abstract
Reactive oxygen species (ROS) plays a key role in the pathogenesis of primary open-angle glaucoma (POAG), a chronic neurodegenerative disease that damages the trabecular meshwork (TM) cells, inducing apoptosis of the retinal ganglion cells (RGC), deteriorating the optic nerve head, and leading to [...] Read more.
Reactive oxygen species (ROS) plays a key role in the pathogenesis of primary open-angle glaucoma (POAG), a chronic neurodegenerative disease that damages the trabecular meshwork (TM) cells, inducing apoptosis of the retinal ganglion cells (RGC), deteriorating the optic nerve head, and leading to blindness. Aqueous humor (AH) outflow resistance and intraocular pressure (IOP) elevation contribute to disease progression. Nevertheless, despite the existence of pharmacological and surgical treatments, there is room for the development of additional treatment approaches. The following review is aimed at investigating the role of different microRNAs (miRNAs) in the expression of genes and proteins involved in the regulation of inflammatory and degenerative processes, focusing on the delicate balance of synthesis and deposition of extracellular matrix (ECM) regulated by chronic oxidative stress in POAG related tissues. The neutralizing activity of a couple of miRNAs was described, suggesting effective downregulation of pro-inflammatory and pro-fibrotic signaling pathways, including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), transforming growth factor-beta 2 (TGF-β2), Wnt/β-Catenin, and PI3K/AKT. In addition, with regards to the elevated IOP in many POAG patients due to increased outflow resistance, Collagen type I degradation was stimulated by some miRNAs and prevented ECM deposition in TM cells. Mitochondrial dysfunction as a consequence of oxidative stress was suppressed following exposure to different miRNAs. In contrast, increased oxidative damage by inhibiting the mTOR signaling pathway was described as part of the action of selected miRNAs. Summarizing, specific miRNAs may be promising therapeutic targets for lowering or preventing oxidative stress injury in POAG patients. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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16 pages, 1276 KiB  
Review
Field Cancerization in NSCLC: A New Perspective on MicroRNAs in Macrophage Polarization
by Radu Pirlog, Andrei Cismaru, Andreea Nutu and Ioana Berindan-Neagoe
Int. J. Mol. Sci. 2021, 22(2), 746; https://doi.org/10.3390/ijms22020746 - 13 Jan 2021
Cited by 15 | Viewed by 4442
Abstract
Lung cancer is currently the first cause of cancer-related death. The major lung cancer subtype is non-small cell lung cancers (NSCLC), which accounts for approximatively 85% of cases. The major carcinogenic associated with lung cancer is tobacco smoke, which produces long-lasting and progressive [...] Read more.
Lung cancer is currently the first cause of cancer-related death. The major lung cancer subtype is non-small cell lung cancers (NSCLC), which accounts for approximatively 85% of cases. The major carcinogenic associated with lung cancer is tobacco smoke, which produces long-lasting and progressive damage to the respiratory tract. The progressive and diffuse alterations that occur in the respiratory tract of patients with cancer and premalignant lesions have been described as field cancerization. At the level of tumor cells, adjacent tumor microenvironment (TME) and cancerized field are taking place dynamic interactions through direct cell-to-cell communication or through extracellular vesicles. These molecular messages exchanged between tumor and nontumor cells are represented by proteins, noncoding RNAs (ncRNAs) and microRNAs (miRNAs). In this paper, we analyze the miRNA roles in the macrophage polarization at the level of TME and cancerized field in NSCLC. Identifying molecular players that can influence the phenotypic states at the level of malignant cells, tumor microenvironment and cancerized field can provide us new insights into tumor regulatory mechanisms that can be further modulated to restore the immunogenic capacity of the TME. This approach could revert alterations in the cancerized field and could enhance currently available therapy approaches. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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11 pages, 1943 KiB  
Review
Role of microRNA and Oxidative Stress in Influenza A Virus Pathogenesis
by Md Mamunul Haque, Dhiraj P. Murale and Jun-Seok Lee
Int. J. Mol. Sci. 2020, 21(23), 8962; https://doi.org/10.3390/ijms21238962 - 25 Nov 2020
Cited by 15 | Viewed by 3084
Abstract
MicroRNAs (miRNAs) are non-coding RNAs that regulate diverse cellular pathways by controlling gene expression. Increasing evidence has revealed their critical involvement in influenza A virus (IAV) pathogenesis. Host–IAV interactions induce different levels of oxidative stress (OS) by disrupting the balance between reactive oxygen [...] Read more.
MicroRNAs (miRNAs) are non-coding RNAs that regulate diverse cellular pathways by controlling gene expression. Increasing evidence has revealed their critical involvement in influenza A virus (IAV) pathogenesis. Host–IAV interactions induce different levels of oxidative stress (OS) by disrupting the balance between reactive oxygen species (ROS) and antioxidant factors. It is thought that miRNA may regulate the expression of ROS; conversely, ROS can induce or suppress miRNA expression during IAV infection. Thus, miRNA and OS are the two key factors of IAV infection and pathogenesis. Accordingly, interactions between OS and miRNA during IAV infection might be a critical area for further research. In this review, we discuss the crosstalk between miRNAs and OS during IAV infection. Additionally, we highlight the potential of miRNAs as diagnostic markers and therapeutic targets for IAV infections. This knowledge will help us to study host–virus interactions with novel intervention strategies. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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54 pages, 3641 KiB  
Review
The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress
by Adam Włodarski, Justyna Strycharz, Adam Wróblewski, Jacek Kasznicki, Józef Drzewoski and Agnieszka Śliwińska
Int. J. Mol. Sci. 2020, 21(18), 6902; https://doi.org/10.3390/ijms21186902 - 20 Sep 2020
Cited by 40 | Viewed by 5505
Abstract
Oxidative stress (OxS) is the cause and the consequence of metabolic syndrome (MetS), the incidence and economic burden of which is increasing each year. OxS triggers the dysregulation of signaling pathways associated with metabolism and epigenetics, including microRNAs, which are biomarkers of metabolic [...] Read more.
Oxidative stress (OxS) is the cause and the consequence of metabolic syndrome (MetS), the incidence and economic burden of which is increasing each year. OxS triggers the dysregulation of signaling pathways associated with metabolism and epigenetics, including microRNAs, which are biomarkers of metabolic disorders. In this review, we aimed to summarize the current knowledge regarding the interplay between microRNAs and OxS in MetS and its components. We searched PubMed and Google Scholar to summarize the most relevant studies. Collected data suggested that different sources of OxS (e.g., hyperglycemia, insulin resistance (IR), hyperlipidemia, obesity, proinflammatory cytokines) change the expression of numerous microRNAs in organs involved in the regulation of glucose and lipid metabolism and endothelium. Dysregulated microRNAs either directly or indirectly affect the expression and/or activity of molecules of antioxidative signaling pathways (SIRT1, FOXOs, Keap1/Nrf2) along with effector enzymes (e.g., GPx-1, SOD1/2, HO-1), ROS producers (e.g., NOX4/5), as well as genes of numerous signaling pathways connected with inflammation, insulin sensitivity, and lipid metabolism, thus promoting the progression of metabolic imbalance. MicroRNAs appear to be important epigenetic modifiers in managing the delicate redox balance, mediating either pro- or antioxidant biological impacts. Summarizing, microRNAs may be promising therapeutic targets in ameliorating the repercussions of OxS in MetS. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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25 pages, 1167 KiB  
Review
Can miRNAs Be Considered as Diagnostic and Therapeutic Molecules in Ischemic Stroke Pathogenesis?—Current Status
by Kirill V. Bulygin, Narasimha M. Beeraka, Aigul R. Saitgareeva, Vladimir N. Nikolenko, Ilgiz Gareev, Ozal Beylerli, Leila R. Akhmadeeva, Liudmila M. Mikhaleva, Luis Fernando Torres Solis, Arturo Solís Herrera, Marco F. Avila-Rodriguez, Siva G. Somasundaram, Cecil E. Kirkland and Gjumrakch Aliev
Int. J. Mol. Sci. 2020, 21(18), 6728; https://doi.org/10.3390/ijms21186728 - 14 Sep 2020
Cited by 36 | Viewed by 4068
Abstract
Ischemic stroke is one of the leading causes of death worldwide. Clinical manifestations of stroke are long-lasting and causing economic burden on the patients and society. Current therapeutic modalities to treat ischemic stroke (IS) are unsatisfactory due to the intricate pathophysiology and poor [...] Read more.
Ischemic stroke is one of the leading causes of death worldwide. Clinical manifestations of stroke are long-lasting and causing economic burden on the patients and society. Current therapeutic modalities to treat ischemic stroke (IS) are unsatisfactory due to the intricate pathophysiology and poor functional recovery of brain cellular compartment. MicroRNAs (miRNA) are endogenously expressed small non-coding RNA molecules, which can act as translation inhibitors and play a pivotal role in the pathophysiology associated with IS. Moreover, miRNAs may be used as potential diagnostic and therapeutic tools in clinical practice; yet, the complete role of miRNAs is enigmatic during IS. In this review, we explored the role of miRNAs in the regulation of stroke risk factors viz., arterial hypertension, metabolic disorders, and atherosclerosis. Furthermore, the role of miRNAs were reviewed during IS pathogenesis accompanied by excitotoxicity, oxidative stress, inflammation, apoptosis, angiogenesis, neurogenesis, and Alzheimer’s disease. The functional role of miRNAs is a double-edged sword effect in cerebral ischemia as they could modulate pathological mechanisms associated with risk factors of IS. miRNAs pertaining to IS pathogenesis could be potential biomarkers for stroke; they could help researchers to identify a particular stroke type and enable medical professionals to evaluate the severity of brain injury. Thus, ascertaining the role of miRNAs may be useful in deciphering their diagnostic role consequently it is plausible to envisage a suitable therapeutic modality against IS. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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25 pages, 1694 KiB  
Review
MicroRNAs Dysregulation and Mitochondrial Dysfunction in Neurodegenerative Diseases
by Mariano Catanesi, Michele d’Angelo, Maria Grazia Tupone, Elisabetta Benedetti, Antonio Giordano, Vanessa Castelli and Annamaria Cimini
Int. J. Mol. Sci. 2020, 21(17), 5986; https://doi.org/10.3390/ijms21175986 - 20 Aug 2020
Cited by 58 | Viewed by 6765
Abstract
Neurodegenerative diseases are debilitating and currently incurable conditions causing severe cognitive and motor impairments, defined by the progressive deterioration of neuronal structure and function, eventually causing neuronal loss. Understand the molecular and cellular mechanisms underlying these disorders are essential to develop therapeutic approaches. [...] Read more.
Neurodegenerative diseases are debilitating and currently incurable conditions causing severe cognitive and motor impairments, defined by the progressive deterioration of neuronal structure and function, eventually causing neuronal loss. Understand the molecular and cellular mechanisms underlying these disorders are essential to develop therapeutic approaches. MicroRNAs (miRNAs) are short non-coding RNAs implicated in gene expression regulation at the post-transcriptional level. Moreover, miRNAs are crucial for different processes, including cell growth, signal transmission, apoptosis, cancer and aging-related neurodegenerative diseases. Altered miRNAs levels have been associated with the formation of reactive oxygen species (ROS) and mitochondrial dysfunction. Mitochondrial dysfunction and ROS formation occur in many neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s diseases. The crosstalk existing among oxidative stress, mitochondrial dysfunction and miRNAs dysregulation plays a pivotal role in the onset and progression of neurodegenerative diseases. Based on this evidence, in this review, with a focus on miRNAs and their role in mitochondrial dysfunction in aging-related neurodegenerative diseases, with a focus on their potential as diagnostic biomarkers and therapeutic targets. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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34 pages, 1421 KiB  
Review
MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases
by Montserrat Climent, Giacomo Viggiani, Ya-Wen Chen, Gerald Coulis and Alessandra Castaldi
Int. J. Mol. Sci. 2020, 21(12), 4370; https://doi.org/10.3390/ijms21124370 - 19 Jun 2020
Cited by 84 | Viewed by 9310
Abstract
Reactive oxygen species (ROS) affect many cellular functions and the proper redox balance between ROS and antioxidants contributes substantially to the physiological welfare of the cell. During pathological conditions, an altered redox equilibrium leads to increased production of ROS that in turn may [...] Read more.
Reactive oxygen species (ROS) affect many cellular functions and the proper redox balance between ROS and antioxidants contributes substantially to the physiological welfare of the cell. During pathological conditions, an altered redox equilibrium leads to increased production of ROS that in turn may cause oxidative damage. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level contributing to all major cellular processes, including oxidative stress and cell death. Several miRNAs are expressed in response to ROS to mediate oxidative stress. Conversely, oxidative stress may lead to the upregulation of miRNAs that control mechanisms to buffer the damage induced by ROS. This review focuses on the complex crosstalk between miRNAs and ROS in diseases of the cardiac (i.e., cardiac hypertrophy, heart failure, myocardial infarction, ischemia/reperfusion injury, diabetic cardiomyopathy) and pulmonary (i.e., idiopathic pulmonary fibrosis, acute lung injury/acute respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, lung cancer) compartments. Of note, miR-34a, miR-144, miR-421, miR-129, miR-181c, miR-16, miR-31, miR-155, miR-21, and miR-1/206 were found to play a role during oxidative stress in both heart and lung pathologies. This review comprehensively summarizes current knowledge in the field. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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23 pages, 382 KiB  
Review
Non-Coding RNA: Role in Gestational Diabetes Pathophysiology and Complications
by Tiziana Filardi, Giuseppina Catanzaro, Stefania Mardente, Alessandra Zicari, Carmela Santangelo, Andrea Lenzi, Susanna Morano and Elisabetta Ferretti
Int. J. Mol. Sci. 2020, 21(11), 4020; https://doi.org/10.3390/ijms21114020 - 04 Jun 2020
Cited by 68 | Viewed by 6552
Abstract
Gestational Diabetes Mellitus (GDM) is defined as glucose intolerance that develops in the second or third trimester of pregnancy. GDM can lead to short-term and long-term complications both in the mother and in the offspring. Diagnosing and treating this condition is therefore of [...] Read more.
Gestational Diabetes Mellitus (GDM) is defined as glucose intolerance that develops in the second or third trimester of pregnancy. GDM can lead to short-term and long-term complications both in the mother and in the offspring. Diagnosing and treating this condition is therefore of great importance to avoid poor pregnancy outcomes. There is increasing interest in finding new markers with potential diagnostic, prognostic and therapeutic utility in GDM. Non-coding RNAs (ncRNAs), including microRNAs, long non-coding RNAs and circular RNAs, are critically involved in metabolic processes and their dysregulated expression has been reported in several pathological contexts. The aberrant expression of several circulating or placenta-related ncRNAs has been linked to insulin resistance and β-cell dysfunction, the key pathophysiological features of GDM. Furthermore, significant associations between altered ncRNA profiles and GDM-related complications, such as macrosomia or trophoblast dysfunction, have been observed. Remarkably, the deregulation of ncRNAs, which might be linked to a detrimental intrauterine environment, can lead to changes in the expression of target genes in the offspring, possibly contributing to the development of long-term GDM-related complications, such as metabolic and cardiovascular diseases. In this review, all the recent findings on ncRNAs and GDM are summarized, particularly focusing on the molecular aspects and the pathophysiological implications of this complex relationship. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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19 pages, 1017 KiB  
Review
Oxidative Stress-Responsive MicroRNAs in Heart Injury
by Branislav Kura, Barbara Szeiffova Bacova, Barbora Kalocayova, Matus Sykora and Jan Slezak
Int. J. Mol. Sci. 2020, 21(1), 358; https://doi.org/10.3390/ijms21010358 - 05 Jan 2020
Cited by 114 | Viewed by 8967
Abstract
Reactive oxygen species (ROS) are important molecules in the living organisms as a part of many signaling pathways. However, if overproduced, they also play a significant role in the development of cardiovascular diseases, such as arrhythmia, cardiomyopathy, ischemia/reperfusion injury (e.g., myocardial infarction and [...] Read more.
Reactive oxygen species (ROS) are important molecules in the living organisms as a part of many signaling pathways. However, if overproduced, they also play a significant role in the development of cardiovascular diseases, such as arrhythmia, cardiomyopathy, ischemia/reperfusion injury (e.g., myocardial infarction and heart transplantation), and heart failure. As a result of oxidative stress action, apoptosis, hypertrophy, and fibrosis may occur. MicroRNAs (miRNAs) represent important endogenous nucleotides that regulate many biological processes, including those involved in heart damage caused by oxidative stress. Oxidative stress can alter the expression level of many miRNAs. These changes in miRNA expression occur mainly via modulation of nuclear factor erythroid 2-related factor 2 (Nrf2), sirtuins, calcineurin/nuclear factor of activated T cell (NFAT), or nuclear factor kappa B (NF-κB) pathways. Up until now, several circulating miRNAs have been reported to be potential biomarkers of ROS-related cardiac diseases, including myocardial infarction, hypertrophy, ischemia/reperfusion, and heart failure, such as miRNA-499, miRNA-199, miRNA-21, miRNA-144, miRNA-208a, miRNA-34a, etc. On the other hand, a lot of studies are aimed at using miRNAs for therapeutic purposes. This review points to the need for studying the role of redox-sensitive miRNAs, to identify more effective biomarkers and develop better therapeutic targets for oxidative-stress-related heart diseases. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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23 pages, 2033 KiB  
Review
Targeting microRNAs as a Therapeutic Strategy to Reduce Oxidative Stress in Diabetes
by Giuseppina Emanuela Grieco, Noemi Brusco, Giada Licata, Laura Nigi, Caterina Formichi, Francesco Dotta and Guido Sebastiani
Int. J. Mol. Sci. 2019, 20(24), 6358; https://doi.org/10.3390/ijms20246358 - 17 Dec 2019
Cited by 30 | Viewed by 5437
Abstract
Diabetes mellitus is a group of heterogeneous metabolic disorders characterized by chronic hyperglycaemia as a consequence of pancreatic β cell loss and/or dysfunction, also caused by oxidative stress. The molecular mechanisms involved inβ cell dysfunction and in response to oxidative stress are also [...] Read more.
Diabetes mellitus is a group of heterogeneous metabolic disorders characterized by chronic hyperglycaemia as a consequence of pancreatic β cell loss and/or dysfunction, also caused by oxidative stress. The molecular mechanisms involved inβ cell dysfunction and in response to oxidative stress are also regulated by microRNAs (miRNAs). miRNAs are a class of negative gene regulators, which modulate pathologic mechanisms occurring in diabetes and its complications. Although several pharmacological therapies specifically targeting miRNAs have already been developed and brought to the clinic, most previous miRNA-based drug delivery methods were unable to target a specific miRNA in a single cell type or tissue, leading to important off-target effects. In order to overcome these issues, aptamers and nanoparticles have been described as non-cytotoxic vehicles for miRNA-based drug delivery. These approaches could represent an innovative way to specifically target and modulate miRNAs involved in oxidative stress in diabetes and its complications. Therefore, the aims of this review are: (i) to report the role of miRNAs involved in oxidative stress in diabetes as promising therapeutic targets; (ii) to shed light onto the new delivery strategies developed to modulate the expression of miRNAs in diseases. Full article
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology 2.0)
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