ArticleFASEB bioAdvances2025
RBM25 Regulates p38 MAPK Pathway Activation via Exon 16 Skipping of MAP4K4 in a Rat Model of Post-Infarction Heart Failure.
Article in FASEB bioAdvances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Harmaline and the gut-brain-immune axis: a novel therapeutic avenue in neuroinflammation and ulcerative colitis.Inflammopharmacology · 2026Review
- Comprehensive analysis of aberrant alternative splicing and RNA binding proteins regulators associated with myocardial ischemia reperfusion injury in mice.Scientific reports · 2026Article
- Dynamic epigenetic and transcriptomic reprogramming during embryonic skin development in goose (Anser anser domesticus).Functional & integrative genomics · 2026Article
- RBM25 Regulates p38 MAPK Pathway Activation via Exon 16 Skipping of MAP4K4 in a Rat Model of Post-Infarction Heart Failure.FASEB bioAdvances · 2025Article
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10 authors.
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Abstract
Ischemic cardiomyopathy remains a leading cause of heart failure (HF), yet its molecular mechanisms remain incompletely defined. This study aimed to identify the RNA-binding protein 25(RBM25) as a critical regulator of HF progression through MAP4K4 alternative splicing and p38 MAPK pathway activation. A left anterior descending (LAD) coronary artery ligation-induced HF model was established in Sprague-Dawley (SD) rats, with pericardial delivery of lentiviral vectors for RBM25 overexpression (OE-RBM25) or shRNA-mediated knockdown (sh-RBM25). Quantitative PCR (qPCR) experiments confirmed that overexpression of RBM25 induces exon 16 skipping in MAP4K4. Computational modeling further predicted that the resulting variant enhances binding to MAP3K1 and potentially activates the MAPK pathway. Cardiac function, infarct size, apoptosis, and molecular markers were evaluated via echocardiography, TTC staining, ELISA, qPCR, Western blot, and TUNEL assays. RBM25 overexpression significantly increased myocardial infarction area compared to the HF control group (
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