AI Article Synopsis
- Iron overload leads to increased reactive oxygen species through the Fenton reaction, causing oxidative stress and potentially resulting in cell death (ferroptosis).
- Diabetes contributes to oxidative stress, inflammation, and other factors that trigger cardiac remodeling and dysfunction, ultimately resulting in diabetic cardiomyopathy (DCM).
- Recent studies highlight the link between iron-induced ferroptosis and DCM, prompting a detailed examination of their mechanisms and implications.
Article Abstract
Iron overload increases the production of harmful reactive oxygen species in the Fenton reaction, which causes oxidative stress in the body and lipid peroxidation in the cell membrane, and eventually leads to ferroptosis. Diabetes is associated with increased intracellular oxidative stress, inflammation, autophagy, microRNA alterations, and advanced glycation end products (AGEs), which cause cardiac remodeling and cardiac diastolic contractile dysfunction, leading to the development of diabetic cardiomyopathy (DCM). While these factors are also closely associated with ferroptosis, more and more studies have shown that iron-mediated ferroptosis is an important causative factor in DCM. In order to gain fresh insights into the functions of ferroptosis in DCM, this review methodically summarizes the traits and mechanisms connected with ferroptosis and DCM.
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| http://dx.doi.org/10.1007/s10741-023-10336-z | DOI Listing |
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