ArticleScientific reports2026
Lactate regulates the YTHDF2-FTH1 axis to promote cardiomyocyte ferroptosis and aggravate myocardial ischemia-reperfusion injury.
Article in Scientific reports, 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
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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.
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Who cites it
1 citing paper in PubMed.
- FTH1 mRNA-Protein Discordance in Cardiac Ferroptosis: Multilayer Posttranscriptional and Degradative Control.Cardiovascular therapeutics · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
Myocardial ischemia–reperfusion (MI/R) injury remains a major clinical challenge, and ferroptosis has recently emerged as a crucial contributor to its pathogenesis. However, the regulatory mechanisms underlying ferroptosis in MI/R remain incompletely understood. Here, we investigated the role of lactate-mediated YTHDF2 regulation in cardiomyocyte ferroptosis. A murine ischemia–reperfusion (I/R) model and an H9C2 hypoxia/reoxygenation (H/R) model were established. Biochemical assays revealed elevated lactate levels in MI/R hearts, accompanied by increased infarct size, enhanced structural damage, and elevated Fe²⁺ and creatine kinase-MB (CK-MB) levels. Lactate treatment promoted YTHDF2 lactylation and upregulated its expression in cardiomyocytes. Mechanistically, YTHDF2 bound to ferritin heavy chain 1 (FTH1) mRNA and reduced its stability through m6A-dependent degradation, thereby promoting ferroptosis. Knockdown of YTHDF2 suppressed ferroptosis, an effect reversed by FTH1 reduction. These findings identify lactate-induced YTHDF2 lactylation as a key driver of cardiomyocyte ferroptosis and reveal a novel mechanism exacerbating MI/R injury, suggesting that targeting this pathway may represent a potential therapeutic strategy.
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Registered trials
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