ArticleAging cell2018
Evidence that miR-146a attenuates aging- and trauma-induced osteoarthritis by inhibiting Notch1, IL-6, and IL-1 mediated catabolism.
Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Efficacy and safety of anti-interleukin-1 therapeutics in the treatment of knee osteoarthritis: a systematic review and meta-analysis of randomized controlled trials.Journal of orthopaedic surgery and research · 2023Pooled it
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- Extracellular Vesicles in Osteoarthritis: From Pathogenic Mediators to Engineered Therapeutics in a Precision Medicine Roadmap.Journal of extracellular biology · 2026Review
- The protective role of CD44 and microRNA-146a in tendinopathy.Bone & joint research · 2026Article
- MicroRNA-mediated mechanotransduction and chondrocyte differentiation in mesenchymal stem cells.Animal cells and systems · 2026Review
- Role of Cytokines in Bone Diseases and Their Therapeutic Application.ImmunoTargets and therapy · 2026Review
- The Notch signaling pathway in regulating bone and cartilage homeostasis: novel insights into the pathogenesis and therapeutics of osteoarthritis.Cell communication and signaling : CCS · 2025Review
- Aging microenvironment in osteoarthritis focusing on early-stage alterations and targeted therapies.Bone research · 2025Review
- Therapeutic Potential of Adipose Mesenchymal Stem Cells for Synovial Regeneration: from In-Vitro Studies to Clinical Applications.Stem cell reviews and reports · 2025Review
- Article
- Therapeutic Effect of Shikimic Acid on Heat Stress-Induced Myocardial Damage: Assessment via Network Pharmacology, Molecular Docking, Molecular Dynamics Simulation, and In Vitro Experiments.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Molecular Signaling Pathways and MicroRNAs in Bone Remodeling: A Narrative Review.Diseases (Basel, Switzerland) · 2024Review
- Nutritional Epigenomics: Bioactive Dietary Compounds in the Epigenetic Regulation of Osteoarthritis.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The Role of MicroRNAs in the Pathophysiology of Osteoarthritis.International journal of molecular sciences · 2024Review
- Inhibition of TLR4 signalling to dampen joint inflammation in osteoarthritis.Rheumatology (Oxford, England) · 2024Review
- Article
- General Control Non-derepressible 2 Alleviates Cartilage Degeneration and Inhibits NLRP3 Inflammasome Activation in Osteoarthritis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Article
- Article
- Circulating miR-146b and miR-27b are efficient biomarkers for early diagnosis of Equidae osteoarthritis.Scientific reports · 2023Article
- Why Does Rehabilitation Not (Always) Work in Osteoarthritis? Does Rehabilitation Need Molecular Biology?International journal of molecular sciences · 2023Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Primary osteoarthritis (OA) is associated with aging, while post-traumatic OA (PTOA) is associated with mechanical injury and inflammation. It is not clear whether the two types of osteoarthritis share common mechanisms. We found that miR-146a, a microRNA-associated with inflammation, is activated by cyclic load in the physiological range but suppressed by mechanical overload in human articular chondrocytes. Furthermore, miR-146a expression is decreased in the OA lesions of human articular cartilage. To understand the role of miR-146a in osteoarthritis, we systemically characterized mice in which miR-146a is either deficient in whole body or overexpressed in chondrogenic cells specifically. miR-146a-deficient mice develop early onset of OA characterized by cartilage degeneration, synovitis, and osteophytes. Conversely, miR-146a chondrogenic overexpressing mice are resistant to aging-associated OA. Loss of miR-146a exacerbates articular cartilage degeneration during PTOA, while chondrogenic overexpression of miR-146a inhibits PTOA. Thus, miR-146a inhibits both OA and PTOA in mice, suggesting a common protective mechanism initiated by miR-146a. miR-146a suppresses IL-1β of catabolic factors, and we provide evidence that miR-146a directly inhibits Notch1 expression. Therefore, such inhibition of Notch1 may explain suppression of inflammatory mediators by miR-146a. Chondrogenic overexpression of miR-146a or intra-articular administration of a Notch1 inhibitor alleviates IL-1β-induced catabolism and rescues joint degeneration in miR-146a-deficient mice, suggesting that miR-146a is sufficient to protect OA pathogenesis by inhibiting Notch signaling in the joint. Thus, miR-146a may be used to counter both aging-associated OA and mechanical injury-/inflammation-induced PTOA.
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What OpenQuestion holds
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.