Advances in biological markers of ferroptosis in myocardial infarction

doi:10.16150/j.1671-2870.2023.02.015

Abstract

Abstract:

The development in diagnosis and treatment of myocardial infarction has significantly improved the prognosis of some patients, while the overall survival rate of patients remains much room for improvement. Further research of the mechanism of injury after myocardial ischemia and reperfusion may explore new directions of research. As a newly discovered form of regulated cell death, ferroptosis, an iron-dependent cell death caused by lipid peroxidation, which has been characterized by cell death involving the accumulation of lipid peroxides and reactive oxygen species. Ferroptosis, which has been acknowledged to play an important role in ischemia-reperfusion injury. Studies suggest that iron death-related marker changes after myocardial infarction (MI), including hiatus of mitochondrial ferritin (FtMt) in intracellular iron metabolism, decreased levels of glutathione peroxidase 4 (Gpx4), a terminal molecule of glutathione metabolism pathway, insufficient use of antiporter cystine/glutathione synthesis (SXc^-) in glutathione synthesis, and overexpression of Acyl-CoA synthetase long-chain family member 4 (ACSL4) can lead to oxidative stress, inflammatory response, cardiomyocyte injury after myocardial infarction, and can aggravate the myocardial ischemia-reperfusion injury. The four biological markers mentioned above, FtMt, Gpx4, SXc^- and ACSL4, are important research targets for the diagnosis and treatment of iron death after MI, which may deserve further study.

Key words: Myocardial infarction, Ferroptosis, Biological marker

CLC Number:

R542.23

CHANG Yuchen, LI Jingbo. Advances in biological markers of ferroptosis in myocardial infarction[J]. Journal of Diagnostics Concepts & Practice, 2023, 22(02): 197-202.

Figures/Tables 3

Table 1

Figure 1

Figure 2

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项目	形态学特征	生化特征
铁死亡	线粒体小而畸形，线粒体嵴减少或消失，细胞膜浓缩，线粒体外膜破裂，细胞核正常	铁代谢异常，脂质过氧化，ROS积累
细胞坏死	质膜破裂、固缩、核裂、核溶解、染色质解体、核轮廓消失和细胞成分溢出	ATP水平降低，DNA随机降解和扩散
细胞凋亡	细胞体积减少，细胞间连接消失，细胞骨架解体，染色质凝集，凋亡小体的形成	Caspase蛋白激活，DNA片段，生物大分子合成
细胞自噬	完整的细胞膜，细胞质中的囊泡样结构和自噬小体的形成	LC3-Ⅱ，P62、Beclin-1蛋白调控
细胞焦亡	细胞肿胀和增大，伴有气泡状突起，细胞膜破裂，内容物流出	炎症小体形成，Gasdermin D蛋白激活，促炎细胞因子释放