Jing Chunlu, Wu Yupeng, Zhang Yuzhu, Zhu Zaihan, Zhang Yong, Liu Zhen, Sun Dandan
Department of Ultrasound, The People's Hospital of China Medical University, The People's Hospital of Liaoning Province, 33 Wenyi Road, Shenhe District, Shenyang, 110067, People's Republic of China.
Shenyang Clinical Medical Research Center for Ultrasound, The People's Hospital of China Medical University, The People's Hospital of Liaoning Province, Shenyang, 110067, People's Republic of China.
Clin Epigenetics. 2025 Jan 11;17(1):4. doi: 10.1186/s13148-024-01809-5.
As an important element of the human body, iron participates in numerous physiological and biochemical reactions. In the past decade, ferroptosis (a form of iron-dependent regulated cell death) has been reported to contribute to the pathogenesis and progression of various diseases. The stability of iron in cardiomyocytes is crucial for the maintenance of normal physiological cardiac activity. Ferroptosis has been detected in many cardiovascular diseases (CVDs), including coronary heart disease, myocardial ischemia-reperfusion injury, heart failure, and chemotherapy-induced myocardial damage. In cardiomyocytes, epigenetic regulation and post-translational modifications regulate the expression of ferroptosis-related factors, maintain iron homeostasis, and participate in the progression of CVDs. Currently, there is no detailed mechanism to explain the relationship between epigenetic regulation and ferroptosis in CVDs. In this review, we provide an initial summary of the core mechanisms of ferroptosis in cardiomyocytes, with first focus on the epigenetic regulation and expression of ferroptosis-related factors in the context of common cardiovascular diseases. We anticipate that the new insights into the pathogenesis of CVDs provided here will inspire the development of clinical interventions to specifically target the active sites of these factors, reducing the harmfulness of ferroptosis to human health.
铁作为人体的重要元素，参与众多生理和生化反应。在过去十年中，有报道称铁死亡（一种铁依赖性调节性细胞死亡形式）与多种疾病的发病机制和进展有关。心肌细胞中铁的稳定性对于维持正常的心脏生理活动至关重要。在许多心血管疾病（CVD）中都检测到了铁死亡，包括冠心病、心肌缺血-再灌注损伤、心力衰竭和化疗引起的心肌损伤。在心肌细胞中，表观遗传调控和翻译后修饰调节铁死亡相关因子的表达，维持铁稳态，并参与心血管疾病的进展。目前，尚无详细机制来解释心血管疾病中表观遗传调控与铁死亡之间的关系。在这篇综述中，我们初步总结了心肌细胞中铁死亡的核心机制，首先关注常见心血管疾病背景下铁死亡相关因子的表观遗传调控和表达。我们预计，本文提供的关于心血管疾病发病机制的新见解将激发针对这些因子活性位点的临床干预措施的开发，减少铁死亡对人类健康的危害。
