ArticleActa Cardiologica Sinica2024
N6-Methyladenosine Demethylase ALKBH5 Promotes Pyroptosis by Modulating PTBP1 mRNA Stability in LPS-Induced Myocardial Dysfunction.
Article in Acta Cardiologica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- m6A RNA methylation in sepsis-induced cardiomyopathy: direct cardiac mechanisms, emerging therapeutic targets, and translational gaps.Frontiers in medicine · 2026Review
- CXCL9 is a dual‑role biomarker in colorectal cancer linked to mitophagy and modulated by ALKBH5.Molecular medicine reports · 2025Article
- Dexmedetomidine plays a protective role in sepsis-associated myocardial injury by repressing PRMT5-mediated ferroptosis.Toxicology research · 2025Article
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2 authors.
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Abstract
Objective: This study aims to investigate the mechanism by which alkB homolog 5 (ALKBH5) regulates polypyrimidine tract-binding protein 1 (PTBP1) to mediate cardiomyocyte pyroptosis in sepsis-induced myocardial injury. Methods: Lipopolysaccharide (LPS)-exposed H9C2 cell and rat models were established to mimic septic myocardial injury both Results: Elevated expressions of both ALKBH5 and PTBP1 were found in the myocardial tissues of LPS-induced septic rats. ALKBH5 knockdown could restore the cell viability and cell pyroptosis inhibited by LPS, while ALKBH5 promoted PTBP1 mRNA stability by affecting its N6-methyladenosine (m6A) modification. Conclusions: ALKBH5 promoted mRNA stability and the expression of PTBP1 through m6A modification to induce pyroptosis in cardiomyocytes and ultimately aggravate sepsis-induced myocardial dysfunction.
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