ArticleJournal of molecular histology2025
Role and mechanism of lncRNA ZEB1-AS1 endogenous competition for miR-365a-3p targeting NRF2 in ferroptosis in articular chondrocytes.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Research progress on the mechanism of chondrocyte ferroptosis in osteoarthritis.Frontiers in immunology · 2026Review
- The "gut microbiota-ferroptosis axis": a hypothesis for osteoarthritis pathogenesis and therapeutic implications.Frontiers in microbiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Osteoarthritis (OA) is an extremely complex chronic whole joint disease. The regulation of NRF2 in cellular ferroptosis is involved in OA development; however, its upstream regulatory mechanism is unclear. Long noncoding RNAs (lncRNAs) regulate the expression of downstream target genes through endogenous competition with micro RNAs. LncRNA ZEB1-AS1 regulates the expression of miR-365a-3p, which in turn negatively regulates NRF2 expression. Both lncRNA ZEB1-AS1 and NRF2 can bind to miR-365a-3p at the same target site. However, it remains unclear whether ZEB1-AS1 could act as a competing endogenous RNA (ceRNA) to reduce miR-365a-3p-mediated inhibition of NRF2. Specifically, the potential mechanism whereby ZEB1-AS1 might sequester miR-365a-3p through competitive binding, thereby alleviating its suppressive effect on NRF2 expression, requires further experimental validation. Therefore, our study aimed to investigate whether lncRNA ZEB1-AS1 could participate in the regulation of NRF2 expression through endogenous competition for binding to miR-365a-3p, as well as the role and mechanism in osteoarthritic cellular ferroptosis. Our findings demonstrated that NRF2 knockdown combined with miR-365a-3p overexpression significantly enhanced cellular ferroptosis and accelerated osteoarthritis progression. Conversely, both miR-365a-3p inhibition and ZEB1-AS1 overexpression were found to upregulate NRF2 expression, thereby mitigating cellular ferroptosis and OA development. Notably, ZEB1-AS1 overexpression exerted dual protective effects in chondrocytes by elevating NRF2 levels, effectively suppressing both ferroptosis and inflammatory damage. Mechanistically, we identified that the lncRNA ZEB1-AS1 modulates OA pathogenesis through the miR-365a-3p/NRF2 axis, suggesting this pathway may serve as a potential therapeutic target for early intervention in OA progression.
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Identifiers
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Registered trials
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