Key result
SGLT2 inhibitors modulate mitochondrial ion transport and ER-mitochondria crosstalk to govern survival in diabetic cardiomyopathy.
This paper reviews the mechanistic role of SGLT2 inhibitors in modulating mitochondrial ion transport and ER-mitochondria crosstalk in the context of diabetic cardiomyopathy.
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MAM disruption in DCM remains preclinical; leaves open whether targeting ER-mitochondria contacts alters patient outcomes.
Diabetic cardiomyopathy (DCM) is a major complication of type 2 diabetes mellitus and a leading contributor to heart failure. A central feature of DCM is the disruption of mitochondrial bioenergetics and calcium homeostasis, processes that are tightly regulated through mitochondria-associated endoplasmic reticulum membranes (MAMs). These ER–mitochondria contact sites coordinate mitochondrial ion transport systems, including the mitochondrial calcium uniporter (MCU), Na⁺/Ca²⁺ exchanger (NCLX), and potassium channels, which collectively govern mitochondrial metabolism, redox balance, and cell survival.
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Flores et al. (2026) conducted a review in Diabetic cardiomyopathy. SGLT2 Inhibitors was evaluated. SGLT2 inhibitors act as modulators of mitochondrial ion transport and ER-mitochondria crosstalk, which govern mitochondrial metabolism and cell survival in diabetic cardiomyopathy.
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