ReviewFrontiers in endocrinology2026
Non-coding RNA in osteoarthritis: mechanistic insights and future perspectives.
Review in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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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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0 citing papers in PubMed.
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Non-coding RNAs (ncRNAs) have emerged as critical regulators of osteoarthritis (OA) pathogenesis by modulating gene expression at the epigenetic, transcriptional, and post-transcriptional levels. Among the major ncRNA classes, microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) regulate key biological processes involved in OA progression, including extracellular matrix degradation, synovial inflammation, chondrocyte apoptosis, autophagy, osteoclastogenesis, and subchondral bone remodeling. Increasing evidence demonstrates that ncRNAs influence multiple OA-associated signaling pathways, particularly NF-κB, TGF-β/SMAD, Wnt/β-catenin, PI3K/Akt, and MAPK/ERK, thereby contributing to cartilage degeneration and the failure of joint homeostasis. This review comprehensively summarizes the current understanding of ncRNA-mediated mechanisms in OA, with an emphasis on mechanistic validation, biomarker development, and therapeutic translation. Among all ncRNA classes, miRNAs currently possess the strongest experimental and translational evidence. miR-140-5p is the most extensively validated cartilage-protective miRNA and suppresses ADAMTS5-mediated extracellular matrix degradation in human OA cartilage, whole-body knockout mouse models, and
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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.