The role and research progress of ferroptosis in myocardial injury in sepsis

Sepsis is triggered by the body's dysregulated response to infection, often accompanied by acute organ dysfunction and a high risk of mortality. The incidence of myocardial injury in sepsis patients ranges from 40% to 70%, with complex pathophysiological mechanisms. In recent years, ferroptosis, a novel form of programmed cell death, has attracted widespread attention. Studies suggest that it may play a key role in sepsis-related myocardial injury; however, research in this field is still in the preliminary stage, with some controversial findings and unclear underlying mechanisms. Notably, risks throughout the perioperative period (preoperative stage, intraoperative trauma/infection, and postoperative recovery) can induce sepsis, which further activates the ferroptosis pathway and leads to myocardial injury. Based on this, integrating ferroptosis into the perioperative management system-optimizing risk stratification through marker screening and implementing targeted interventions-holds great significance for reducing the risk of perioperative sepsis-related myocardial injury. This article systematically summarizes the latest research progress on ferroptosis in sepsis-related myocardial injury, explores its potential mechanisms, and screens for potential therapeutic targets by combining the characteristics of perioperative risks, thereby providing references for subsequent clinical research and practice.