ArticleBioscience reports2020
miR-122/SIRT1 axis regulates chondrocyte extracellular matrix degradation in osteoarthritis.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular Mechanisms Involved.International journal of molecular sciences · 2025Review
- Role and mechanism of lncRNA ZEB1-AS1 endogenous competition for miR-365a-3p targeting NRF2 in ferroptosis in articular chondrocytes.Journal of molecular histology · 2025Article
- LATS1-modulated ZBTB20 perturbing cartilage matrix homeostasis contributes to early-stage osteoarthritis.Bone research · 2025Article
- Lnc-HULC, miR-122, and sirtulin-1 as potential diagnostic biomarkers for psoriasis and their association with the development of metabolic syndrome during the disease course.Non-coding RNA research · 2023Article
- Matrix metalloproteinases in rheumatoid arthritis and osteoarthritis: a state of the art review.Reumatologia · 2023Review
- Chelidonine reduces IL-1β-induced inflammation and matrix catabolism in chondrocytes and attenuates cartilage degeneration and synovial inflammation in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
- Interaction between SIRT1 and non-coding RNAs in different disorders.Frontiers in genetics · 2023Review
- Potential Methods of Targeting Cellular Aging Hallmarks to Reverse Osteoarthritic Phenotype of Chondrocytes.Biology · 2022Review
- The therapeutic effect and mechanism of melatonin on osteoarthritis: From the perspective of non-coding RNAs.Frontiers in genetics · 2022Review
- Longevity-Promoting Pathways and Transcription Factors Respond to and Control Extracellular Matrix Dynamics During Aging and Disease.Frontiers in aging · 2022Review
- Review
- The non-coding RNA interactome in joint health and disease.Nature reviews. Rheumatology · 2021Review
- Article
- Data Integration Reveals the Potential Biomarkers of Circulating MicroRNAs in Osteoarthritis.Diagnostics (Basel, Switzerland) · 2021Review
- Roflumilast Reduced the IL-18-Induced Inflammatory Response in Fibroblast-Like Synoviocytes (FLS).ACS omega · 2021Article
- Febuxostat mitigates IL-18-induced inflammatory response and reduction of extracellular matrix gene.American journal of translational research · 2021Article
- Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis.Frontiers in cell and developmental biology · 2021Review
- Roflumilast prevents lymphotoxin α (TNF-β)-induced inflammation activation and degradation of type 2 collagen in chondrocytes.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- β-ecdysterone alleviates osteoarthritis by activating autophagy in chondrocytes through regulating PI3K/AKT/mTOR signal pathway.American journal of translational research · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsMicroRNAs (miRNAs) are involved in the pathogenesis of osteoarthritis (OA). The present study aimed to investigate the potential function of miR-122 in the development of OA and its potential molecular mechanisms.
methodsThe expression of miR-122, silent information regulator 1 (SIRT1), collagen II, aggrecan, matrix metalloproteinase (MMP) 13 (MMP13) and ADAMTS4 in OA cartilage was detected by RT-qPCR. Target gene prediction and screening, luciferase reporter assay were used to verify downstream target genes of miR-122.
resultsCompared with osteonecrosis, the expression of miR-122 was significantly increased in OA cartilage, while the expression of SIRT1 was significantly decreased. Overexpression of miR-122 increased the expression of extracellular matrix (ECM) catabolic factors, for example disintegrins, MMPs and metalloproteinases with platelet reaction protein motifs, and inhibited the expression of synthetic metabolic genes such as collagen II and aggregating proteoglycan. Inhibition of miR-122 expression had the opposite effect. Furthermore, SIRT1 was identified as a direct target of miR-122. SIRT1 was significantly inhibited by miR-122 overexpression. Knockdown of SIRT1 reversed the degradation of chondrocyte ECM by miR-122 inhibitors.
conclusionThe miR-122/SIRT1 axis can regulate the degradation of ECM in OA, thus providing new insights into the treatment of OA.
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