Fig. 8

Schematic diagram summarizing the protective effects of irisin treatment in type 1 diabetic cardiomyopathy through anti-ferroptosis via induction of the SIRT1-p53-SLC7A11/GPX4 pathway. High glucose, a key pathogenic factor of DCM of the type 1 diabetic model, increases intracellular Fe²⁺ and lipid peroxidation, along with GSH depletion and SLC7A11(cystine/glutamate antiporter)/GPX4 inhibition, implying a role for ferroptosis in the pathogenesis of T1DM. Irisin suppresses ferroptosis and alleviates cardiac remodeling and dysfunction via activation of the SIRT1-p53-SLC7A11/GPX4 pathway. DCM, diabetic cardiomyopathy, SLC7A11 solute carrier family 7 member 11, GPX4 glutathione peroxidase 4, Ac acetylation, GSH reduced glutathione, and SIRT1 Sirtuin 1