ReviewFrontiers in cardiovascular medicine2025
Ferroptosis and protein translation: emerging perspectives in the research of myocardial infraction.
Review in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
- Extracellular Vesicles in Myocardial Infarction: Dual Role in Ferroptosis Regulation and In Vivo Imaging.Diagnostics (Basel, Switzerland) · 2026Review
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Authors and funding
10 authors.
Funding
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Abstract
Myocardial infarction, as the principal type of ischemic heart disease, has currently become the focus of research on its prevention and treatment strategies. From the perspective of myocardial infarction pathogenesis, it is urgent to impede the progression of this disease and improve diagnosis and treatment techniques. Ferroptosis, a form of programmed cell death mechanistically distinct from apoptosis and autophagy, is implicated throughout the pathogenesis of myocardial infarction. Dysregulation of protein translation leads to abnormal protein expression, disruption of cellular signaling, and cell dysfunction, thereby disturbing normal cellular function and exacerbating disease progression. Consequently, clarifying the mechanism of protein translation dysregulation in ferroptosis during myocardial infarction will enhance the understanding of the pathogenesis of myocardial infarction. In this review, the latest research progress in the relationship between protein translation and ferroptosis is collected. The mechanisms by which they regulate myocardial infarction are explored, and the current research status of the role of protein translation in different stages of ferroptosis is introduced. These findings are expected to provide valuable insights for clarifying the pathophysiological mechanisms of myocardial infarction and for precise treatment.
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