The sodium‐glucose co‐transporter‐2 inhibitor ertugliflozin modifies the signature of cardiac substrate metabolism and reduces cardiac <scp>mTOR</scp> signalling, endoplasmic reticulum stress and apoptosis

Abstract

SGLT2 inhibition reduced left ventricular fibrosis in a murine model of cardiac hypertrophy. Mechanistically, this was associated with reduced cardiac insulin and increased AMPK signalling as a potential mechanism for less cardiac mTOR activation with alleviation of downstream ER stress, UPR and apoptosis.