Search Results (7,903)

Acute Kidney Injury (AKI) is a critical medical condition characterized by a sudden and significant decline in renal function over a short timeframe. Commonly triggered by factors such as sepsis, ischemia–reperfusion injury, or nephrotoxic agents, AKI is linked to substantial rates of morbidity and mortality. In recent years, small non-coding RNAs have gained attention as promising biomarkers for the early diagnosis and potential treatment of AKI. Among them, microRNAs (miRNAs)—short RNA sequences of 21–25 nucleotides that regulate gene expression via sequence-specific binding—stand out due to their remarkable stability in biological fluids such as plasma and urine. Notably, certain miRNAs, including miR-21, miR-30, miR-494, and miR-29, have shown the ability to detect AKI earlier than traditional biomarkers like serum creatinine, offering the potential to enhance clinical decision-making. This narrative review aims to provide a comprehensive overview of the recent findings regarding the involvement of non-coding RNA, in particular microRNAs, in both the early diagnosis and therapeutic strategies for AKI. By highlighting their potential as sensitive biomarkers and novel treatment targets, this review seeks to contribute to advancing clinical approaches that improve patient outcomes. Ultimately, a deeper understanding and utilization of microRNAs could lead to the development of new diagnostic tools and targeted therapies for AKI, helping to prevent progression to chronic kidney disease and reduce associated mortality rates. However, further clinical studies and translational applications are still needed to validate these findings and implement them in patient care. Full article

Rheumatoid arthritis (RA) is a prevalent autoimmune disease characterized by chronic joint inflammation. Its pathophysiology involves complex interactions among immune cells, leading to joint damage, primarily in the synovial membrane. MicroRNAs (miRs), single-stranded non-coding RNAs, play a critical role in regulating pathways affecting RA progression, particularly in fibroblast-like synoviocytes and peripheral blood mononuclear cells. Key pathways influenced by miRs include NF-κB, apoptosis, PI3K/AKT signaling, and cytokine production. Dysregulated miRs impact cell proliferation, survival, and inflammatory responses. This review explores not only the role of miRs in RA pathogenesis, but also highlights their potential as biomarkers for early detection and severity prediction. Moreover, therapeutic approaches targeting miRs, including mimics and inhibitors, show promise in animal models, with methods like intra-articular administration being favored due to better efficacy and reduced side effects. While early studies highlight potential pathways for RA treatment, challenges remain in translating these findings into safe and effective clinical therapies. Full article

Mollusks, such as bivalves, face increasing threats, such as disease, in aquaculture. Exosomes, widely derived from living cells carrying diverse bioactive molecules, affect the immune response. To overcome these challenges, bivalves utilize exosomal miRNAs as critical regulators of immune responses. This study investigates the role of exosomal miRNAs in modulating immune and metabolic responses in Pinctada fucata martensii following lipopolysaccharide (LPS) stimulation. Exosomes (75–150 nm) were isolated from hemolymph and characterized. High-throughput sequencing identified 30 differentially expressed miRNAs (DEMs) and 1349 differentially expressed genes (DEGs) in LPS-treated oysters, with significant enrichment in TNF, TLR/NF-κB, and metabolic pathways. This study revealed exosomal miRNA-mediated regulation of immune genes (IκBα, TRAF6, IRAK1, and BIRC2/3) and metabolic enzymes (PCK and CYP2J), demonstrating their role in apoptosis, inflammation, and metabolic reprogramming. Network analysis highlighted miRNA–mRNA interactions, including miR-7/IκBα (TNF pathway) and miR-34_5/IRAK1 (TLR pathway). Additionally, exosomal miRNAs (miR-92_2 and novel_mir5) were found to regulate oxidative stress (SOD1) and gluconeogenesis (PCK), linking immune defense with metabolic adaptation. These findings provide novel insights into exosomal miRNA-mediated immune regulation in bivalves, revealing conserved mechanisms with potential implications for molluscan health and disease management. Full article

As sessile organisms, plants have developed strategies to cope with exposure to high radiation. The plant cuticle is located at the interface between the plant and the surrounding environment, thus acting as a first barrier that protects plants against environmental conditions, including solar radiation. The isolated cuticles displayed notable absorptance in the infrared spectral range which, according to Kirchhoff’s law of thermal radiation, equals the emission dissipation ability. Comparison among the different cuticles showed that a significant range of their reflectance, transmittance, and absorbance spectra match the spectral regions known as atmospheric windows, between 3–4 and 8–13 microns, located within the mid-infrared region (MIR). They allow energy to pass through into the outer space. These optical parameters varied between cuticles from different plant species and they were not a simple function of the cuticle’s thickness but the product of its specific composition in combination with its molecular arrangement. Full article

Focal cortical dysplasia (FCD) is a major cause of drug-resistant epilepsy, yet its molecular basis remains poorly understood. Numerous studies have analyzed RNA, protein, and microRNA alterations, but results are often inconsistent across subtypes and methodologies. To address this gap, we conducted a systematic review integrating transcriptomic, proteomic, and microRNA data from 117 human studies of FCD subtypes I–III. Differentially expressed factors were extracted, categorized by subtype, and analyzed using pathway enrichment and network approaches. Our integrative analysis revealed convergent dysregulation of neuroinflammatory, synaptic, cytoskeletal, and metabolic pathways across FCD subtypes. Consistently altered genes, including IL1B, TLR4, BDNF, HMGCR, and ROCK2, together with dysregulated microRNAs such as hsa-miR-21-5p, hsa-miR-155-5p, and hsa-miR-132-3p, were linked to PI3K–Akt–mTOR, Toll-like receptor, and GABAergic signaling, emphasizing shared pathogenic mechanisms. Importantly, we identified overlapping transcript–protein patterns and subtype-specific molecular profiles that may refine diagnosis and inform therapeutic strategies. This review provides the first cross-omics molecular framework of FCD, demonstrating how convergent pathways unify heterogeneous findings and offering a roadmap for biomarker discovery and targeted interventions. Full article

High temperatures are one of the most important abiotic stressors affecting the survival and growth of American shad (Alosa sapidissima). Building on previous omics sequencing studies of A. sapidissima liver and gills under high temperature stress, this study focused on investigating the regulatory role of miR-1236-3p and its target gene hsp90b1. The results indicate that the full-length cDNA of the hsp90b1 gene is 2023 bp and comprises a 5’ end of 58 bp, a 3’ end of 84 bp, and a coding region of 1881 bp, encoding 626 amino acids. Sequence alignment and phylogenetic tree analysis reveal that the hsp90b1 sequence is highly conserved across species. In situ hybridization showed that hsp90b1 is mainly localized in the cytoplasm. Software prediction identified a potential binding site between miR-1236-3p and hsp90b1. Through the construction of wild-type and mutant 3’UTR hsp90b1 dual luciferase reporter plasmids, the targeted relationship between the two was confirmed. In addition, the spatiotemporal expression levels of the hsp90b1 was found to be highest in the multicellular stage and liver tissue at a cultivation temperature of 27 °C; miR-1236-3P was highly expressed in the hatching stage and heart tissue at 30 °C. These findings provide a theoretical foundation for further investigating the regulatory role of non-coding RNA in A. sapidissima heat stress and offer data for subsequent molecular breeding studies. Full article

MicroRNA-22 (miR-22) is a negative regulator of mitochondrial biogenesis, as well as lipid and glucose metabolism, in metabolically active tissues. Silencing miR-22 holds promise as a potential treatment of obesity and metabolic syndrome, as it restores metabolic capacity—enhancing oxidative metabolism—and reduces ectopic fat accumulation in chronic obesity, a driver of impaired metabolic flexibility and muscle mass loss. Intramuscular adipose accumulation and defective mitochondrial function are features associated with obese-mediated muscle atrophy and hallmarks of neuromuscular disorders such as Duchenne muscular dystrophy. Therefore, miR-22 could represent a compelling molecular target to improve muscle health across various muscle-wasting conditions. This study describes a pharmacological strategy for the inhibition of miR-22 in skeletal muscle by employing a mixmer antisense oligonucleotide (ASO, anti-miR-22). Administration of the ASO in a mouse model of obesity positively modulated myogenesis while protecting dystrophic mice from muscle function decline, enhancing fatigue resistance, and limiting pathological fibrotic remodeling. Mechanistically, we show that anti-miR-22 treatment promotes derepression of genes involved in mitochondrial homeostasis, favoring oxidative fiber content regardless of the disease model, thus promoting a more resilient phenotype. Furthermore, we suggest that miR-22 inhibition increases autophagy by transcriptional activation of multiple negative regulators of mammalian target of rapamycin (mTOR) signaling to decrease immune infiltration and fibrosis. These findings position miR-22 as a promising therapeutic target for muscle atrophy and support its potential to restore muscle health. Full article

This study investigated the role of miR-144 in mitigating oxidized fish oil (OFO)-induced muscle oxidative stress and quality deterioration in Megalobrama amblycephala. The feeding trial was conducted for 5 weeks, and four experimental diets were formulated, namely NC (fresh fish oil), OF (OFO), OF + ago (OFO and miR-144 agomir), and OF + anta (OFO and miR-144 antagomir). Histological results showed that OFO significantly reduced myofiber density (from 758.00 ± 13.69 to 636.57 ± 13.44 N/mm²) and decreased the percentage of myofibers with diameters > 50 μm (from 53.45% to 38.52%). OFO intake significantly increased the content of malondialdehyde (MDA), protein carbonyl (PC), advanced oxidation protein product (AOPP), and 3-nitrotyrosine (3-NT), and significantly decreased superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity in muscle. OFO treatment significantly up-regulated the expression of inflammatory factors (NF-κB, TNF-α, HO-1, and IL-6), significantly down-regulated NQO1. Moreover, OFO reduced muscle differentiation and maturation by down-regulating the expression of MyoG, MYHC1, and protein synthesis genes (AKT3, TOR, and S6K1), and up-regulating the expression of protein hydrolysis genes (FoxO3a, MuRF1, HSP70, Beclin-1, P62, and ATG8). Moreover, miR-144 agomir exacerbated OFO-induced muscle damage by suppressing Nrf2, whereas miR-144 antagomir mitigated these effects. Silencing miR-144 re-activates Nrf2, alleviating oxidative damage, enhancing protein deposition, and improving muscle quality. These findings suggest that targeting the miR-144/Nrf2 axis could counteract OFO-induced muscle deterioration. Full article

Asthma is a chronic respiratory disease affecting over 262 million people worldwide, with obesity-associated asthma emerging as a distinct endotype of increasing prevalence characterized by metabolic inflammation and airway remodeling. Unlike allergic asthma, this phenotype is driven by chronic low-grade inflammation, originating from hypertrophic and hypoxic adipose tissue. This dysregulated state leads to the activation of pro-inflammatory pathways and the secretion of cytokines, contributing to airway dysfunction and remodeling. Recent evidence highlights non-coding RNAs (ncRNAs) as key regulators of these processes. MicroRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) influence inflammation and remodeling by modulating immune cell polarization, cytokine secretion, extracellular matrix composition, and airway smooth muscle cell (ASMC) proliferation. Notably, H19, MEG3, GAS5, miR-26a-1-3p, and miR-376a-3p have been implicated in both asthma and obesity, suggesting their role in linking metabolic dysfunction with airway pathology. Moreover, ncRNAs regulate Treg/Th17 balance, fibroblast activation, and autophagy-related pathways, further influencing airway remodeling. Our in silico analysis highlighted the IGF1R signaling pathway as a key enriched mechanism, linking selected ncRNAs with metabolic dysregulation and inflammation in obesity-related asthma. This paper reviews how ncRNAs regulate inflammation and airway remodeling in obesity-associated asthma, emphasizing their potential molecular links between metabolic dysfunction and airway pathology. Full article

Background: Cardiometabolic syndromes, including diabetes, obesity, and metabolic syndrome, significantly contribute to cardiovascular fibrosis, a major driver of heart failure. Non-coding RNAs (ncRNAs)—notably microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs)—have emerged as critical epigenetic regulators of fibrotic remodeling. Recent studies indicate that widely used metabolic modulators can influence ncRNA expression, potentially impacting on cardiovascular fibrosis. This review synthesizes evidence on the interplay between metabolic therapies and ncRNA regulation, with emphasis on therapeutic and biomarker potential of miRNAs. Methods: A literature search was manually curated and conducted on PubMed for studies published mainly in the last decade and evaluating the effects of metformin, sodium-glucose cotransporter-2 (SGLT2) inhibitors, peroxisome proliferator-activated receptor gamma (PPARγ) agonists, glucagon-like peptide 1 (GLP-1) receptor agonists, and fatty acid oxidation inhibitors on ncRNA expression in the context of cardiovascular fibrosis. Data from in vitro, in vivo, and clinical studies were extracted and categorized by drug class, ncRNA target, and functional outcomes. Results: Several metabolic modulators specifically downregulate pro-fibrotic (miR-21, miR-92, H19, and metastasis associated lung adenocarcinoma transcript 1 (MALAT1)) and upregulate anti-fibrotic ncRNAs (miR-29, miR-133a, miR-711, miR-133a, miR-30a and miR-200 family). This results in global attenuation of the transforming growth factor- beta (TGF-β) signaling, which limits extracellular matrix (ECM) accumulation thus improving myocardial compliance. Across drug classes, changes in ncRNA profiles paralleled improvements in fibrosis-related endpoints. Conclusions: Metabolic modulators exert anti-fibrotic effects partly through ncRNA regulation, offering novel therapeutic strategies and potential biomarkers for cardiovascular fibrosis in cardiometabolic disease. Targeting metabolic–ncRNA crosstalk may enable more precise and synergistic interventions for preventing or reversing pathological remodeling. Full article

The original purpose of this study was to compare human and pig scRNA-seq data to determine why pigs do not have brown adipocytes. However, during the experiment, we identified brown adipocytes in pigs. Therefore, we aimed to confirm that these adipocytes were brown adipocytes via a comparative analysis using typical mouse brown adipose tissue sections. We found that swine brown adipocytes were distributed in an island-like pattern, with three typical characteristics: (1) numerous mitochondria and small lipid droplets, (2) a cellular volume smaller than that of white adipocytes, and (3) expression of specific marker genes (EBF2 and ATP2B4). The expression levels of the thermogenesis-related genes UCP2/3 were not significantly increased. Thus, we conducted ceRNA network analysis, revealing that high expression of the key microRNA miR-10383 increased the thermogenic efficiency of UCP3 in the cold exposure group. In addition, the epigenetic memory of UCP3 was disrupted. Chromatin accessibility and Whole-Transcriptome Sequencing of Groin Adiposesibility results revealed peaks in the promoter regions of the UCP2/3 genes. In our discussion of the study’s limitations, we explain how to repeat the experiment to significantly increase the UCP2/3 protein content. This study fills a research gap regarding brown fat in pigs and can provide a reference for future studies on fat metabolism. Full article

Background/Objectives: Neurodegenerative diseases (NDs) such as Alzheimer’s (AD), Parkinson’s (PD), Huntington’s (HD), and Amyotrophic Lateral Sclerosis (ALS) are clinically distinct but share overlapping molecular mechanisms. Methods: To identify conserved systemic signatures, we analyzed blood RNA-Seq datasets using Weighted Gene Co-Expression Network Analysis (WGCNA), differential expression, pathway enrichment, and miRNA–mRNA network mapping. Results: Two modules, the red and turquoise, showed strong preservation across diseases. The red module was enriched for cytoskeletal and metabolic regulation, while the turquoise module involved immune, stress-response, and proteostatic pathways. Discussion: Key hub genes, such as HMGCR, ACTR2, MYD88, PTEN, EP300, and regulatory miRNAs like miR-29, miR-132, and miR-146a, formed interconnected networks reflecting shared molecular vulnerabilities. The absence of classical heat shock proteins in preserved blood modules highlights tissue-specific expression differences between blood and neural systems. Several hub genes overlap with known pharmacological targets, suggesting potential in translational relevance. Conclusions: Together, these findings reveal conserved blood-based transcriptional modules that suggest parallel central neurodegenerative processes and may support future biomarker development and possible therapeutic exploration. Full article

Background: Immunodeficiencies are a heterogeneous group of disorders classified etiologically as primary (congenital) or secondary (acquired). Primary immunodeficiencies (PIDs), such as common variable immunodeficiency (CVID), result from genetic mutations that impair the development and function of lymphocytes. Secondary immunodeficiencies (SIDs) arise as a consequence of chronic diseases, lymphoid malignancies, or immunosuppressive therapies. Aim of the study: The purpose of this study was to assess the serum expression profile of selected microRNAs (miRNAs) in patients with CVID and in those with chronic lymphocytic leukemia (CLL) and coexisting SID, compared to healthy individuals. Methods: Digital PCR (dPCR) was applied to quantify the serum expression levels of selected miRNAs in patients with CVID, patients with CLL and SID, and in healthy controls. Results: dPCR revealed significantly reduced levels of miR-16, miR-30c, miR-181a, miR-29a, miR-150, and miR-326 in the CVID group, potentially reflecting impaired regulatory mechanisms of the immune system. In contrast, elevated levels of miR-21, miR-125b, and miR-155 were observed in the CLL group with SID, suggesting their role in tumorigenesis and secondary immunosuppression. Correlations between miRNA levels and the expression of immune checkpoints (PD-1, CTLA-4, CD200) indicated the involvement of a complex regulatory network encompassing both humoral and cellular immune mechanisms. Conclusions: The results provide preliminary evidence that selected miRNAs could reflect disease-specific immune dysregulation patterns and may hold potential as diagnostic and prognostic biomarkers in both PIDs and SIDs. Full article

This study explores the use of mid-infrared (MIR) free-electron laser (FEL) irradiation as a tool for tailoring the surface properties of electrochemically synthesized TiO₂—graphene quantum dots (QDs). The QDs, prepared in colloidal form via a cost-effective electrochemical method in a KCl—citric acid medium, were exposed to MIR wavelengths (5.76, 8.02, and 9.10 µm) at the Kyoto University FEL facility. Post-irradiation measurements revealed a pronounced inversion of zeta potential by 40–50 mV and approximately 10% reduction in hydrodynamic size, indicating double-layer contraction and ionic redistribution at the QD—solvent interface. Photoluminescence spectra showed enhanced emission for GQDs and TiO₂/GQD composites, while Tauc analysis revealed modest bandgap blue shifts (0.04–0.08 eV), both consistent with trap-state passivation and sharper band edges. TEM confirmed intact crystalline structures, verifying that FEL-induced modifications were confined to surface chemistry rather than bulk lattice damage. Taken together, these results demonstrate that MIR FEL irradiation provides a resonance-driven, non-contact method to reorganize ions, suppress defect states, and improve the optoelectronic quality of QDs. This approach offers a scalable post-synthetic pathway for enhancing electron transport layers in perovskite solar cells and highlights the broader potential of photonic infrastructure for advanced nanomaterial processing and interface engineering in optoelectronic and energy applications. Full article