Update on the potential role and its regulatory mechanism of iron metabolism and ferroptosis of cardiomyocytes in cardiomyopathy

• Published in: 生物医学转化 Vol. 2; no. 4; pp. 27 - 33
• Main Authors: Li Jingyan, Tian Yingping, Yao Yongming
• Format: Journal Article
• Language: Chinese
• Published: Lanzhou University Press 01.12.2021
• Subjects: cardiomyocyte; cardiomyopathy; cell death; ferroptosis; ironmetabolism
• ISSN: 2096-8965
• DOI: 10.12287/j.issn.2096-8965.20210404

It has been demonstrated that cardiomyocyte metabolism and cell death are the fundamental progresses in the development of cardiomyopathy. Increasing evidences suggest that metabolic imbalance of iron appears to be involved in the pathophysiology of cardiomyopathy. As we well known, iron is an essential mineral required for various functions, including cellular respiration, lipid and oxygen metabolism, as well as protein synthesis. However, cardiomyocyte homeostasis and viability are inclined to be jeopardized by iron-induced toxicity under pathological stress, which is defined as ferroptosis. In the pathogenesis of cardiomyopathy, excessive iron is transported into cells that drives cardiomyocytes more vulnerable to ferroptosis by the accumulation of reactive oxygen species through Fenton reaction. The enhanced induction of reactive oxygen species in ferroptosis leads cardiomyocytes to become more sensitive to oxidative stress under the exposure of excess iron. Thus, ferroptosis might play an important role