ArticleBone & joint research2026
The protective role of CD44 and microRNA-146a in tendinopathy.
Article in Bone & joint research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
1 citing paper in PubMed.
- Decoding miRNA‑146a: Mechanisms of action in cardiovascular diseases and endocrine metabolic disorders (Review).International journal of molecular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims: Tendinopathy is a pathological condition characterized by pain and significant dysfunction, with its pathogenesis involving various factors including chronic inflammation, cellular senescence, and apoptosis. Previous research indicates that blocking CD44 signalling exacerbates apoptosis and inflammation in tendinopathic tenocytes. Furthermore, microRNA-146a (miR-146a) has been shown to counteract interleukin-1β (IL)-1β-induced senescence in these cells, and is upregulated by CD44 in knee osteoarthritis. Therefore, this study aimed to investigate the CD44-miR-146a signalling axis in regulating apoptosis in tendinopathy. Methods: Lentiviral vectors (LVs) were used to overexpress CD44 cDNA (LVCD44) and miR-146a precursor (LVmiR-146a) in rat primary tendinopathic tenocytes and tendons. Apoptosis was assessed using terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining. To dissect the CD44-AKT-miR-146a signalling pathway, the PI3K/AKT inhibitor LY294002 and the CD44 antagonizing antibody OX-50 were used. In situ hybridization (ISH) and immunohistochemistry (IHC) were performed to examine the pathway's effect on Smad4 expression in tendinopathic tenocytes and tendons. Results: Overexpression of CD44 and miR-146a in tendinopathic tenocytes resulted in significantly reduced apoptosis compared to controls. The CD44-AKT-miR-146a signalling axis was found to mitigate apoptosis in IL-1β-stimulated tenocytes and in a rat model of collagenase-induced Achilles tendinopathy, primarily by suppressing Smad4 expression. Conclusion: This study highlights the protective role of the CD44-AKT-miR-146a axis in tendinopathy. By modulating the AKT/miR-146a/Smad4 signalling pathway, CD44 and miR-146a effectively reduce apoptosis in tendinopathic tenocytes and tendons.
Identifiers
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.