Septic cardiomyopathy is one of the predominant culprit factors contributing to the rising mortality in patients with severe sepsis. Among various mechanisms responsible for the etiology of septic heart anomalies, disruption of mitochondrial homeostasis has gained much recent attention, resulting in myocardial inflammation and even cell death. Ferroptosis is a novel category of regulated cell death (RCD) provoked by iron-dependent phospholipid peroxidation through iron-mediated phospholipid (PL) peroxidation, enroute to the rupture of plasma membranes and eventually cell death. This review summarizes the recent progress of ferroptosis in mitochondrial homeostasis during septic cardiomyopathy. We will emphasize the role of mitochondrial iron transport channels and the antioxidant system in ferroptosis. Finally, we will summarize and discuss future research, which should help guide disease treatment.

脓毒症心肌病是导致严重脓毒症患者死亡率上升的主要原因之一。在导致脓毒症心脏异常病因的多种机制中，线粒体稳态的破坏最近引起了人们的广泛关注，导致心肌炎症甚至细胞死亡。铁死亡是一类新型的调节性细胞死亡（RCD），由铁介导的磷脂（PL）过氧化作用引起的铁依赖性磷脂过氧化作用，导致质膜破裂并最终导致细胞死亡。本文总结了脓毒症心肌病期间铁死亡在线粒体稳态中的最新进展。我们将强调线粒体铁转运通道和抗氧化系统在铁死亡中的作用。最后，我们将总结并讨论未来的研究，这应该有助于指导疾病治疗。