# Ferroptosis and protein translation: emerging perspectives in the research of myocardial infraction

## TL;DR

This review explores how protein translation and ferroptosis contribute to heart attack progression and treatment.

## Contribution

It summarizes recent findings on the interplay between protein translation and ferroptosis in myocardial infarction.

## Key findings

- Ferroptosis plays a key role in the pathogenesis of myocardial infarction.
- Dysregulated protein translation disrupts cellular signaling and worsens disease progression.
- Understanding these mechanisms may lead to improved treatment strategies for heart attacks.

## 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.