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Ferroptosis: Roles and Molecular Mechanisms in Diabetic Cardiomyopathy

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Specialty Endocrinology
Date 2023 May 8
PMID 37152931
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Abstract

Diabetic cardiomyopathy (DCM) is a serious complication of type 1 and type 2 diabetes, which leads to the aggravation of myocardial fibrosis, disorders involving systolic and diastolic functions, and increased mortality of patients with diabetes through mechanisms such as glycolipid toxicity, inflammatory response, and oxidative stress. Ferroptosis is a form of iron-dependent regulatory cell death that is attributed to the accumulation of lipid peroxides and an imbalance in redox regulation. Increased production of lipid reactive oxygen species (ROS) during ferroptosis promotes oxidative stress and damages myocardial cells, leading to myocardial systolic and diastolic dysfunction. Overproduction of ROS is an important bridge between ferroptosis and DCM, and ferroptosis inhibitors may provide new targets for the treatment of patients with DCM.

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References
1.
Sung M, Hamza S, Dyck J . Myocardial metabolism in diabetic cardiomyopathy: potential therapeutic targets. Antioxid Redox Signal. 2015; 22(17):1606-30. DOI: 10.1089/ars.2015.6305. View

2.
Wang S, Zhu S, Wu J, Zhang M, Xu Y, Xu W . Exercise enhances cardiac function by improving mitochondrial dysfunction and maintaining energy homoeostasis in the development of diabetic cardiomyopathy. J Mol Med (Berl). 2020; 98(2):245-261. DOI: 10.1007/s00109-019-01861-2. View

3.
Wang D, Liu K, Zhong J, Li X, Zhang J, Wang G . Molecular Correlates of Early Onset of Diabetic Cardiomyopathy: Possible Therapeutic Targets. Oxid Med Cell Longev. 2022; 2022:9014155. PMC: 9023181. DOI: 10.1155/2022/9014155. View

4.
Li W, Li W, Leng Y, Xiong Y, Xia Z . Ferroptosis Is Involved in Diabetes Myocardial Ischemia/Reperfusion Injury Through Endoplasmic Reticulum Stress. DNA Cell Biol. 2019; 39(2):210-225. DOI: 10.1089/dna.2019.5097. View

5.
Hansen S, Aasum E, Hafstad A . The role of NADPH oxidases in diabetic cardiomyopathy. Biochim Biophys Acta Mol Basis Dis. 2017; 1864(5 Pt B):1908-1913. DOI: 10.1016/j.bbadis.2017.07.025. View