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by directing the activation of fibroblasts, EMT, and ECM remodeling, miRNAs exert pivotal regulatory control over fibrotic disease progression, and this multi-pathway capability positions them as a major focus of antifibrotic research (109)

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470 In animal models of Apelin-13-caused cardiomyocyte hypertrophy and heart failure, NCOA4-activated ferritinophagy leads to the upregulation of SFXN1 expression, causing mitochondrial iron overload and mitochondrial ROS overproduction, increased lipid peroxidation, and ultimately, ferroptosis