ArticleCell death & disease2018
MicroRNA-128a represses chondrocyte autophagy and exacerbates knee osteoarthritis by disrupting Atg12.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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.
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Pooled it
- Review
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- Gene Therapy for the Treatment of Osteoarthritis: Advances and Prospective.Current pharmaceutical design · 2026Review
- The dual role of autophagy in cartilage degradation: from mechanisms to targeted therapeutics.Frontiers in cell and developmental biology · 2026Review
- Urinary long non-coding RNA GAS5 as a noninvasive diagnostic biomarker for renal fibrosis.Renal failure · 2025Article
- Targeting EZH2 in autoimmune diseases: unraveling epigenetic regulation and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Gold Nanoparticles as a Tool to Detect Biomarkers in Osteoarthritis: New Insights.Indian journal of microbiology · 2025Article
- Landscape of Histone Posttranslational Modifications in Osteoarthritis.Journal of inflammation research · 2025Review
- Review
- Matrix stiffness aggravates osteoarthritis progression through H3K27me3 demethylation induced by mitochondrial damage.iScience · 2024Article
- Gubi decoction mitigates knee osteoarthritis via promoting chondrocyte autophagy through METTL3-mediated ATG7 mJournal of cellular and molecular medicine · 2024Article
- The Role of MicroRNAs in the Pathophysiology of Osteoarthritis.International journal of molecular sciences · 2024Review
- CircRNA SEC24A promotes osteoarthritis through miR-107-5p/CASP3 axis.Regenerative therapy · 2024Article
- The emerging roles of miRNA-mediated autophagy in ovarian cancer.Cell death & disease · 2024Review
- Intra-articular administration of PLGA resveratrol sustained-release nanoparticles attenuates the development of rat osteoarthritis.Materials today. Bio · 2024Article
- Orchestrating Cellular Balance: ncRNAs and RNA Interactions at the Dominant of Autophagy Regulation in Cancer.International journal of molecular sciences · 2024Review
- Chondrocyte autophagy mechanism and therapeutic prospects in osteoarthritis.Frontiers in cell and developmental biology · 2024Review
- Curculigoside inhibits osteoarthritis <em>via</em> the regulation of NLRP3 pathway.European journal of histochemistry : EJH · 2023Article
- Rheumatoid Arthritis Has Won the Battle but Not the War: How Many Joints Will We Save Tomorrow?Medicina (Kaunas, Lithuania) · 2023Review
6 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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chondrocyte loss is a prominent feature of osteoarthritis (OA). Autophagy is indispensable in maintaining the metabolic activities of cells exposed to deleterious stress. The contribution of microRNA signaling to chondrocyte autophagy in OA development remains elusive. We uncovered an association between poor autophagy and increased miR-128a expressions in articular chondrocytes of patients with end-stage knee OA and in a rat anterior cruciate ligament transection (ACLT) model for OA development. Cartilage matrix degradation and severe OA histopathology was evident upon forced miR-128a expression within the articular compartment. Intra-articular injections with miR-128a antisense oligonucleotide stabilized chondrocyte autophagy and slowed ACLT-mediated articular tissue destruction, including cartilage erosion, synovitis, osteophyte formation, and subchondral plate damage. In vitro, miR-128 signaling hindered Atg12 expression, LC3-II conversion, and autophagic puncta formation through targeting the 3'-untranslated region of Atg12. It increased apoptotic programs, diminishing cartilage formation capacity of articular chondrocytes. Inactivating histone methyltransferase EZH2 reduced methyl histone H3K27 enrichment in the miR-128a promoter and upregulated miR-128a transcription in inflamed chondrocytes. Taken together, miR-128a-induced Atg12 loss repressed chondrocyte autophagy to aggravate OA progression. EZH2 inactivation caused H3K27 hypomethylation to accelerate miR-128a actions. Interruption of miR-128a signaling attenuated chondrocyte dysfunction and delayed OA development. Our data provide new insights into how miR-128a signaling affects chondrocyte survival and articular cartilage anabolism and highlight the potential of miR-128a targeting therapy to alleviate knee OA.
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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.