Signal Transduction and Targeted Therapy (Aug 2022)
Cardiomyocyte-specific knockout of ADAM17 ameliorates left ventricular remodeling and function in diabetic cardiomyopathy of mice
Abstract
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.