ArticleNature communications2022
Dual functions of microRNA-17 in maintaining cartilage homeostasis and protection against osteoarthritis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 116 citations in OpenAlex.
- Targeting Osteoporosis-Osteoarthritis Comorbidity: Multi-Omics Identification of SON and Exploration of Therapeutic Agents.International journal of molecular sciences · 2026Article
- Harnessing bi-exosome combination alleviates osteoarthritis progression.Bioactive materials · 2026Article
- Review
- Mesenchymal stem cell-derived miR-125b-1-3p-abundant exosomes alleviate osteoarthritis by modulating the KDM6B-H3K27me3-FOXM1 axis.Journal of orthopaedic surgery and research · 2026Article
- α-Ketoglutarate protects against cartilage damage via epigenetically driven metabolic reprogramming in osteoarthritis models.The Journal of clinical investigation · 2026Article
- The use of molecular cues to regenerate musculoskeletal tissues.Innovative surgical sciences · 2026Review
- Dual metabolic-inflammation modulation in MicroRNA@neutrophil-derived microvesicles achieve robust osteoarthritis therapy.Acta pharmaceutica Sinica. B · 2026Article
- Lubricin in osteoarthritis: functions and therapeutic prospects.Frontiers in immunology · 2026Review
- Loss of the miR-221/222 Cluster Promotes the Pathogenesis of Osteoarthritis in Inflamed Mouse Chondrocytes and Osteoarthritis Models.Inflammation · 2025Article
- A bio-adaptive physical hydrogel enables dynamic tissue engineering for tracheal reconstruction.Nature communications · 2025Article
- miRNA-130b-3p upregulation impairs osteogenic differentiation in AIS patients by inhibiting the IGF1/ERK pathway.Cellular and molecular life sciences : CMLS · 2025Article
- Molecular Pathogenesis of Joint Hypermobility: The Role of Intergenic Interactions.Medical sciences (Basel, Switzerland) · 2025Article
- Inhibition of Heat Shock Protein 90β by Catalpol: A Potential Therapeutic Approach for Alleviating Inflammation-Induced Cartilage Injuries in Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Engineered Stem Cell Clusters for Extracellular Vesicles-Mediated Gene Delivery to Rejuvenate Chondrocytes and Facilitate Chondrogenesis in Osteoarthritis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Current cutting-edge omics techniques on musculoskeletal tissues and diseases.Bone research · 2025Review
- Unraveling the brain-joint axis: genetic, transcriptomic, and cohort insights from neuroticism to osteoarthritis.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- ATF1 and miR-27b-3p drive intervertebral disc degeneration through the PPARG/NF-κB signaling axis.Communications biology · 2025Article
- Streamlined metal-based hydrogel facilitates stem cell differentiation, extracellular matrix homeostasis and cartilage repair in male rats.Nature communications · 2025Article
- Recent advances in omics and the integration of multi-omics in osteoarthritis research.Arthritis research & therapy · 2025Review
- Investigation of MicroRNA-17 Expression, Tumor Necrosis Factor-α, and Interleukin-6 Levels in Lumbar Degenerative Disc Disease: Case-Control Study.Journal of clinical medicine · 2025Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damaged hyaline cartilage has no capacity for self-healing, making osteoarthritis (OA) "difficult-to-treat". Cartilage destruction is central to OA patho-etiology and is mediated by matrix degrading enzymes. Here we report decreased expression of miR-17 in osteoarthritic chondrocytes and its deficiency contributes to OA progression. Supplementation of exogenous miR-17 or its endogenous induction by growth differentiation factor 5, effectively prevented OA by simultaneously targeting pathological catabolic factors including matrix metallopeptidase-3/13 (MMP3/13), aggrecanase-2 (ADAMTS5), and nitric oxide synthase-2 (NOS2). Single-cell RNA sequencing of hyaline cartilage revealed two distinct superficial chondrocyte populations (C1/C2). C1 expressed physiological catabolic factors including MMP2, and C2 carries synovial features, together with C3 in the middle zone. MiR-17 is highly expressed in both superficial and middle chondrocytes under physiological conditions, and maintains the physiological catabolic and anabolic balance potentially by restricting HIF-1α signaling. Together, this study identified dual functions of miR-17 in maintaining cartilage homeostasis and prevention of OA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.