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Antioxidants
Special Issues
Mitochondrial Oxidative Stress in Kidney Injury
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Mitochondrial Oxidative Stress in Kidney Injury

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 9416

Special Issue Editor

Dr. Sandra Rayego-Mateos

E-Mail Website
Guest Editor
Molecular and Cellular Biology in Renal and Vascular Pathology, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid Faculty of Medicine, Madrid, Spain
Interests: chronic kidney disease (CKD); acute kidney injury (AKI); glomerular damage; renal inflammation; renal fibrosis; tubular damage
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Kidney disease, including chronic kidney disease (CKD) and acute kidney injury (AKI), has been established as one of the public health priorities due to its high prevalence in the population, their strong impact on the quality of patients' life, and their elevated economic cost. Mitochondria are dynamic and heterogeneous organelles that are the most important source of oxidative stress and adenosine triphospate (ATP) production, regulating redox homeostasis in the cell environment. In addition, this organelle participates in metabolic signaling pathways such as fatty acid β-oxidation,Ca2+ homeostasis, proliferation, and apoptosis. CKD and AKI have a common link, which is the generation of free radicals and reactive oxygen species (ROS) when renal damage appears. There are several processes regulating the mitochondria conditions, such as mitochondrial biogenesis/turnover (mitonuclear network); dynamics (fusion/fission process), bioenergetics (OXPHOS respiratory chain) and autophagy (mytophagy). In the pathological progression of renal damage, all these regulating mitochondrial processes become dysfunctional, contributing to respiratory chain derived oxidative stress that gives place to inflammation, fibrosis, and kidney failure, hence the importance of analyzing mitochondrial biology and its pathological features to develop therapeutic options in renal diseases.

We invite you to submit your latest research studies or a review article concerning mitochondrial damage and oxidation in renal diseases, including AKI and CKD. We welcome submissions concerning all forms of mitochondrial dysfunction in mitochondrial biogenesis/turnover; dynamics, bioenergetics and mytophagy. We believe that this Special Issue, “Mitochondrial Oxidative Stress in Kidney Injury”, will help to highlight the most recent advances in all aspects of the exacerbation of ROS production by mitochondrial dysfunction in renal damage.

Dr. Sandra Rayego-Mateos
Guest Editor

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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • Mitochondrial damage
  • Oxidative stress
  • Chronic kidney disease (CKD)
  • Acute kidney injury (AKI)
  • Renal inflammation
  • Renal fibrosis

Published Papers (3 papers)

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Research

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19 pages, 3910 KiB  
Article
BET Protein Inhibitor JQ1 Modulates Mitochondrial Dysfunction and Oxidative Stress Induced by Chronic Kidney Disease
by Sandra Rayego-Mateos, Pamela Basantes, José Luis Morgado-Pascual, Beatriz Brazal Prieto, Beatriz Suarez-Alvarez, Alberto Ortiz, Carlos Lopez-Larrea and Marta Ruiz-Ortega
Antioxidants 2023, 12(5), 1130; https://doi.org/10.3390/antiox12051130 - 20 May 2023
Cited by 1 | Viewed by 1586
Abstract
Among the mechanisms involved in the progression of kidney disease, mitochondrial dysfunction has special relevance. Epigenetic drugs such as inhibitors of extra-terminal domain proteins (iBET) have shown beneficial effects in experimental kidney disease, mainly by inhibiting proliferative and inflammatory responses. The impact of [...] Read more.
Among the mechanisms involved in the progression of kidney disease, mitochondrial dysfunction has special relevance. Epigenetic drugs such as inhibitors of extra-terminal domain proteins (iBET) have shown beneficial effects in experimental kidney disease, mainly by inhibiting proliferative and inflammatory responses. The impact of iBET on mitochondrial damage was explored in in vitro studies in renal cells stimulated with TGF-β1 and in vivo in murine unilateral ureteral obstruction (UUO) model of progressive kidney damage. In vitro, JQ1 pretreatment prevented the TGF-β1-induced downregulation of components of the oxidative phosphorylation chain (OXPHOS), such as cytochrome C and CV-ATP5a in human proximal tubular cells. In addition, JQ1 also prevented the altered mitochondrial dynamics by avoiding the increase in the DRP-1 fission factor. In UUO model, renal gene expression levels of cytochrome C and CV-ATP5a as well as protein levels of cytochrome C were reduced These changes were prevented by JQ1 administration. In addition, JQ1 decreased protein levels of the DRP1 fission protein and increased the OPA-1 fusion protein, restoring mitochondrial dynamics. Mitochondria also participate in the maintenance of redox balance. JQ1 restored the gene expression of antioxidant proteins, such as Catalase and Heme oxygenase 1 in TGF-β1-stimulated human proximal tubular cells and in murine obstructed kidneys. Indeed, in tubular cells, JQ1 decreased ROS production induced by stimulation with TGF-β1, as evaluated by MitoSOXTM. iBETs, such as JQ1, improve mitochondrial dynamics, functionality, and oxidative stress in kidney disease. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Kidney Injury)
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14 pages, 6201 KiB  
Article
Hot Water Extract of Sasa borealis (Hack.) Makino & Shibata Abate Hydrogen Peroxide-Induced Oxidative Stress and Apoptosis in Kidney Epithelial Cells
by Ilekuttige Priyan Shanura Fernando, Kirinde Gedara Isuru Sandanuwan Kirindage, Arachchige Maheshika Kumari Jayasinghe, Eui Jeong Han, Mawalle Kankanamge Hasitha Madhawa Dias, Kyung Pil Kang, Sung Ig Moon, Tai Sun Shin, Ayeong Ma, Kyungsook Jung and Ginnae Ahn
Antioxidants 2022, 11(5), 1013; https://doi.org/10.3390/antiox11051013 - 20 May 2022
Viewed by 2494
Abstract
Sasa borealis (Hack.) Makino & Shibata or broad-leaf bamboo is famous for its richness of bioactive natural products and its uses in traditional medicine for its anti-inflammatory, diuretic, and antipyretic properties and preventive effects against hypertension, arteriosclerosis, cardiovascular disease, and cancer. The present [...] Read more.
Sasa borealis (Hack.) Makino & Shibata or broad-leaf bamboo is famous for its richness of bioactive natural products and its uses in traditional medicine for its anti-inflammatory, diuretic, and antipyretic properties and preventive effects against hypertension, arteriosclerosis, cardiovascular disease, and cancer. The present study investigated the antioxidant activity of S. borealis hot water extract (SBH) and its effects in ameliorating hydrogen peroxide-induced oxidative stress, using an African green monkey kidney epithelial cell line (Vero). Known polyphenols in SBH were quantified by HPLC analysis. SBH indicated a dose-dependent increase for reducing power, ABTS+ (IC50 = 96.44 ± 0.61 µg/mL) and DPPH (IC50 = 125.78 ± 4.41 µg/mL) radical scavenging activities. SBH markedly reduced intracellular reactive oxygen species (ROS) generation in the Vero cells and increased the protective effects against H2O2-induced oxidative stress by reducing apoptosis. Other than the direct involvement in neutralizing ROS, metabolites in SBH were also found to induce NRF2-mediated production of antioxidant enzymes, HO-1, and NQO1. These findings imply that S. borealis hot water extract can be utilized to create nutraceutical and functional foods that can help to relieve the effects of oxidative stress in both acute and chronic kidney injury. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Kidney Injury)
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Review

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19 pages, 1100 KiB  
Review
Klotho, Oxidative Stress, and Mitochondrial Damage in Kidney Disease
by Javier Donate-Correa, Beatriz Martín-Carro, Jorge B. Cannata-Andía, Carmen Mora-Fernández and Juan F. Navarro-González
Antioxidants 2023, 12(2), 239; https://doi.org/10.3390/antiox12020239 - 20 Jan 2023
Cited by 20 | Viewed by 4559
Abstract
Reducing oxidative stress stands at the center of a prevention and control strategy for mitigating cellular senescence and aging. Kidney disease is characterized by a premature aging syndrome, and to find a modulator targeting against oxidative stress, mitochondrial dysfunction, and cellular senescence in [...] Read more.
Reducing oxidative stress stands at the center of a prevention and control strategy for mitigating cellular senescence and aging. Kidney disease is characterized by a premature aging syndrome, and to find a modulator targeting against oxidative stress, mitochondrial dysfunction, and cellular senescence in kidney cells could be of great significance to prevent and control the progression of this disease. This review focuses on the pathogenic mechanisms related to the appearance of oxidative stress damage and mitochondrial dysfunction in kidney disease. In this scenario, the anti-aging Klotho protein plays a crucial role by modulating signaling pathways involving the manganese-containing superoxide dismutase (Mn-SOD) and the transcription factors FoxO and Nrf2, known antioxidant systems, and other known mitochondrial function regulators, such as mitochondrial uncoupling protein 1 (UCP1), B-cell lymphoma-2 (BCL-2), Wnt/β-catenin, peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1 alpha), transcription factor EB, (TFEB), and peroxisome proliferator-activated receptor gamma (PPAR-gamma). Therefore, Klotho is postulated as a very promising new target for future therapeutic strategies against oxidative stress, mitochondria abnormalities, and cellular senescence in kidney disease patients. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Kidney Injury)
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