3.2.1 Ferroptosis is involved in the occurrence of AF
Iron overload and oxidative stress are essential pathological processes
in ferroptosis. Studies have confirmed that iron overload and oxidative
stress affect cardiac pathophysiology and can lead to
AF79,80. Nomani et al. found that AF was more common
in beta-thalassemia patients than in the normal population, for whom
iron overload of the heart and iron-dependent oxidative stress is one of
the most important causes of atrial fibrillation81.
Iron overload is related to AF occurrence. It was found that AF was
induced by chronic iron overload79. FPN mediates iron
efflux, an important protein that regulates iron and calcium homeostasis
in cells. After knocking out FPN, rats’ intracellular iron concentration
and oxidative stress were further increased, and AF was more likely to
be induced12.
Oxidative stress is associated with AF occurrence. In myocardial tissue,
elevated ROS levels are associated with AF. Elevated ROS levels lead to
protein, lipid, and DNA damage, and are also involved in cardiac
structural and electrical remodeling, increasing susceptibility to
AF82,83. Connexin distribution and protein level
changes were associated with enhanced AF
susceptibility84. Studies have found that ROS may
induce AF by decreasing the expression of connexin 40 and connexin
4385.
Given the above basis, it has been confirmed that ferroptosis occurs in
AF. This study pointed out that cardiac fibroblasts promote the
ferroptosis of cardiomyocytes by secreting exosomes, and reduce the loss
of cardiomyocytes and oxidative stress damage by interfering with
exosome miRNA, which can prevent the continuous development of
AF6.