ArticleCells2019
MicroRNA-34a and MicroRNA-181a Mediate Visfatin-Induced Apoptosis and Oxidative Stress via NF-κB Pathway in Human Osteoarthritic Chondrocytes.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 73 citations in OpenAlex.
- A sulfate-arsenical-ferruginous water affects apoptosis, oxidative stress and the gene expression of inflammatory mediators and of a panel of MicroRNA in IL-1β stimulated human osteoarthritic chondrocytes.Frontiers in medicine · 2026Article
- The Nrf2/HO-1 signaling pathway in arthritis: from molecular mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Expression of Serum and Exosomal microRNA-34a in Subjects with Increased Fat Mass.International journal of molecular sciences · 2025Article
- Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular Mechanisms Involved.International journal of molecular sciences · 2025Review
- Visfatin promotes multiple myeloma cell proliferation and inhibits apoptosis by inducing IL-6 production via NF-κB pathways.Discover oncology · 2025Article
- Oxidative stress in diabetes mellitus and its complications: From pathophysiology to therapeutic strategies.Chinese medical journal · 2025Review
- Mitochondrial bioenergetics dysfunction in T2DM: linking oxidative stress to insulin resistance.Frontiers in endocrinology · 2025Review
- Regulating lipid metabolism in osteoarthritis: a complex area with important future therapeutic potential.Annals of medicine · 2024Review
- The Role of Adipokines between Genders in the Pathogenesis of Osteoarthritis.International journal of molecular sciences · 2024Review
- ROS-induced imbalance of the miR-34a-5p/SIRT1/p53 axis triggers chronic chondrocyte injury and inflammation.Heliyon · 2024Article
- Ethanolic Extract of Propolis Modulates Autophagy-Related microRNAs in Osteoarthritic Chondrocytes.International journal of molecular sciences · 2023Article
- Recent Therapeutic Strategies for Excessive Chondrocyte Death in Osteoarthritis: A Review.Orthopaedic surgery · 2023Review
- Antioxidative Effects of Black Currant and Cornelian Cherry Juices in Different Tissues of an Experimental Model of Metabolic Syndrome in Rats.Antioxidants (Basel, Switzerland) · 2023Article
- Extracellular vesicle-microRNAs mediated response of bovine ovaries to seasonal environmental changes.Journal of ovarian research · 2023Article
- The miR-181 family: Wide-ranging pathophysiological effects on cell fate and function.Journal of cellular physiology · 2023Review
- Costunolide alleviates hyperglycaemia-induced diabetic cardiomyopathy via inhibiting inflammatory responses and oxidative stress.Journal of cellular and molecular medicine · 2023Article
- Extracellular nicotinamide phosphoribosyltransferase: role in disease pathophysiology and as a biomarker.Frontiers in immunology · 2023Review
- Exerkines and osteoarthritis.Frontiers in physiology · 2023Review
- Mitochondrial-targeting MnRegenerative biomaterials · 2023Article
- The protective activity of natural flavonoids against osteoarthritis by targeting NF-κB signaling pathway.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current evidence suggests a complex interaction between adipokines and microRNA (miRNA) in osteoarthritis (OA) pathogenesis. The present study explored the role of miR-34a and miR-181a in regulating apoptosis and oxidative stress induced by visfatin in human OA chondrocytes. Chondrocytes were transfected with miR-34a and miR-181a inhibitors and stimulated with visfatin for 24 h, in the presence of nuclear factor (NF)-κB inhibitor (BAY-11-7082, 2 h pre-incubation). Apoptosis and reactive oxygen species (ROS) production were detected by cytometry, miRNA, antioxidant enzymes, nuclear factor erythroid (NRF)2 and B-cell lymphoma (BCL)2 expressions by quantitative real time polymerase chain reaction (real time PCR) and western blot. P50 NF-κB subunit was measured by immunofluorescence. Visfatin significantly induced apoptosis and superoxide anion production, increased miR-34a, miR-181a, superoxide dismutase (SOD)-2, catalase (CAT), NRF2 and decreased BCL2 gene and protein expression in OA chondrocytes. All the visfatin-caused effects were suppressed by using miR-34a and miR-181a inhibitors. Pre-incubation with BAY-11-7082 counteracted visfatin-induced expression of miRNA, BCL2, SOD-2, CAT and NRF2. Inhibition of miR-34a and miR-181a significantly reduced the activation of p50 NF-κB. Visfatin confirms its ability to induce apoptosis and oxidative stress in human OA chondrocytes; these effects appeared mediated by miR-34a and miR-181a via NF-κB pathway. We highlight the relevance of visfatin as potential therapeutic target for OA treatment.
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Registered trials
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