Abstract
Ferroptosis is a recently identified cell death characterized by an excessive accumulation of iron-dependent reactive oxygen species (ROS) and lipid peroxides. Intracellular iron overload can not only cause damage to macrophages, endothelial cells, and cardiomyocytes through responses such as lipid peroxidation, oxidative stress, and inflammation, but can also affect cardiomyocyte Ca2+ handling, impair excitation–contraction coupling, and play an important role in the pathological process of heart failure with preserved ejection fraction (HFpEF). However, the mechanisms through which ferroptosis initiates the development and progression of HFpEF have not been established. This review explains the possible correlations between HFpEF and ferroptosis and provides a reliable theoretical basis for future studies on its mechanism.
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