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Proposed mechanisms underlying the salutary effects of ADAM17 deficiency on diabetic cardiomyopathy. ADAM17 deficiency increases autophagosome formation and improves autophagic flux via reducing ACE2 shedding, activating AMPK pathway, and promoting TFEB nuclear translocation, which reduces the apoptotic response in cardiomyocytes and attenuates left ventricular remodeling and dysfunction in DCM of mice.