ArticleJournal of cellular and molecular medicine2026
OIP5-AS1 Sponges miR-223-3p to Upregulate FoxO3 and Ameliorate Temporomandibular Joint Osteoarthritis by Inhibiting Chondrocyte Apoptosis.
Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Apoptosis and functional loss of articular chondrocytes serve as initiating events in temporomandibular joint osteoarthritis (TMJOA), and FoxO3 represents a critical molecule for sustaining chondrocyte homeostasis. This study investigates the regulatory mechanism of the lncRNA-OIP5-AS1/hsa-miRNA-223-3p/FoxO3 axis in TMJOA, aiming to identify potential therapeutic targets for this disease. Single-cell database analysis first revealed markedly reduced FoxO3 expression in TMJOA-derived chondrocytes. A rat TMJOA model was then constructed and assigned to control, model, and FoxO3 overexpression groups; micro-CT and histological staining, including HE and Safranin O-fast green staining, were applied to assess articular cartilage injury, while immunohistochemistry was used to detect cartilage-associated proteins Col2a1, MMP-13, Aggrecan, and ADAMTS-5. Further in vitro experiments validated the chondroprotective function of FoxO3 as well as the binding interaction between FoxO3 and rno-miRNA-223-3p. Database screening confirmed significant down-regulation of FoxO3 in TMJOA cartilage. Animal experiments demonstrated that FoxO3 overexpression mitigated chondrocyte injury in rat TMJOA lesions, increased Col2a1 and Aggrecan levels, and suppressed MMP-13 and ADAMTS-5 expression. Cellular assays showed that FoxO3 overexpression enhanced chondrocyte proliferation and matrix synthesis and preserved chondrocyte function. Sequencing and cellular evidence indicated that rno-miRNA-223-3p directly targets FoxO3 mRNA to repress its transcription and negatively modulate FoxO3 abundance, consequently aggravating chondrocyte apoptosis. Collectively, rno-miRNA-223-3p suppresses FoxO3 activity to facilitate TMJOA pathogenesis, and the lncRNA-OIP5-AS1/rno-miRNA-223-3p/FoxO3 regulatory cascade may act as a promising molecular target for TMJOA clinical intervention.
Indexed as
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.