ArticleBMC musculoskeletal disorders2023
Upregulating miR-181b promotes ferroptosis in osteoarthritic chondrocytes by inhibiting SLC7A11.
Article in BMC musculoskeletal disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Blood-based microRNAs as the potential biomarkers for Alzheimer's disease: evidence from a systematic review.Metabolic brain disease · 2024Pooled it
- Ferroptosis-Driven Senescence Loop as a Central Amplifier of Osteoarthritis Progression.Biomolecules & therapeutics · 2026Review
- Aging at the Crossroads of Cuproptosis and Ferroptosis: From Molecular Pathways to Age-Related Pathologies and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Programmed cell death in degenerative skeletal diseases: molecular crosstalk and combinatorial therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- Phosphatidylethanolamine Alleviates Osteoarthritis Progression by Inhibiting Oxidative Stress-Induced Chondrocyte Ferroptosis in a Lysosomal-Dependent Manner.International journal of general medicine · 2026Article
- Exploring the Therapeutic Potential of MIR-140-3p in Osteoarthritis: Targeting CILP and Ferroptosis for Novel Treatment Strategies.Cell proliferation · 2025Article
- Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular Mechanisms Involved.International journal of molecular sciences · 2025Review
- MicroRNA-181a/b-1 enhances chondroprogenitor anabolism and downregulates aquaporin-9.Osteoarthritis and cartilage open · 2025Article
- Chondrocyte Ferritinophagy as a Molecular Mechanism of Arthritis-A Narrative Review.Cell biochemistry and biophysics · 2025Review
- Ferroptosis at the intersection of osteoarthritis and bone metabolism: mechanistic links and therapeutic prospects.Frontiers in cell and developmental biology · 2025Review
- Glutathione peroxidase 4 as an emerging therapeutic target in osteoarthritis: focus on ferroptosis.Frontiers in cell and developmental biology · 2025Review
- Molecular Mechanisms of Immunoinflammatory Infiltration and Ferroptosis in Arthritis Revealed by a Combination of Bioinformatics and Single-Cell Analysis.Journal of inflammation research · 2025Article
- Nanoagent-Mediated Photothermal Therapy: From Delivery System Design to Synergistic Theranostic Applications.International journal of nanomedicine · 2025Review
- Ferroptosis in Arthritis: Driver of the Disease or Therapeutic Option?International journal of molecular sciences · 2024Review
- Regulation of ferroptosis in osteoarthritis and osteoarthritic chondrocytes by typical MicroRNAs in chondrocytes.Frontiers in medicine · 2024Review
- The modulation of immune cell death in connection to microRNAs and natural products.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOsteoarthritis (OA) is a common disease with a complex pathology. This study aimed to investigate the correlation between the aberrant upregulation of miR-181b and ferroptosis in chondrocytes during the progression of OA.
methodsAn OA cell model was constructed with erastin. Ferrostatin-1 (Fer), bioinformatics, and dual-luciferase activity reports were used to investigate the effect of miR-181b on OA. Finally, a rat model of OA was induced by monosodium iodoacetate to verify that miR-181b inhibits SLC7A11 gene expression and increases ferroptosis.
resultsThe results showed that Fer could effectively reverse the erastin-induced inhibition of human chondrocyte viability, increase the level of collagenous proteins in human chondrocytes, and inhibit oxidative stress and ferroptosis. MiR-181b is abnormally elevated in OA cell models. Transfection of a miR-181b inhibitor could increase the expression levels of the ferroptosis-related proteins solute carrier family 7 members 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), thereby inhibiting the occurrence of ferroptosis in chondrocytes. In addition, hsa-miR-181b-5p and SLC7A11 have a targeted regulatory effect. Transfection of SLC7A11 siRNA effectively abrogated the increase in chondrocyte viability induced by the miR-181 inhibitor and increased ferroptosis. Finally, miR-181b was shown to exacerbate OA disease progression by inhibiting SLC7A11 gene expression and increasing ferroptosis in a rat OA model.
conclusionsElevating miR-181b may mediate chondrocyte ferroptosis by targeting SLC7A11 in OA.
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