ArticleFrontiers in physiology2026
Direct dapagliflozin exposure enhances respiration and membrane hyperpolarization in isolated cardiac mitochondria.
Article in Frontiers in physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Dapagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor widely used for the treatment of diabetes, has been consistently associated with cardiovascular protection, including attenuation of ischemia/reperfusion injury and reduced incidence of heart failure. However, the cellular and molecular mechanisms underlying these effects remain incompletely understood. In this context, the present study aimed to investigate whether dapagliflozin exerts direct effects on mitochondrial function and bioenergetics. Cardiac mitochondria were isolated from Wistar rats (Rattus norvegicus), and mitochondrial function was systematically evaluated by assessing oxygen consumption, ATP production, reactive oxygen species (ROS) generation, and mitochondrial membrane potential following exposure to dapagliflozin (10 nM). Dapagliflozin increased oxygen consumption in states 1-3 supported by complex I substrates and enhanced both basal and ADP-stimulated respiration in complex II, without affecting state 4 respiration, complex IV activity, or maximal uncoupled respiration. In parallel, dapagliflozin significantly reduced mitochondrial ROS production in both complexes I and II without altering ATP generation, resulting in an increased ATP/ROS ratio, indicative of improved bioenergetic efficiency. Notably, electron leakage was increased in complex I but remained unchanged in complex II, suggesting differential modulation of electron transport chain components. Furthermore, dapagliflozin induced mitochondrial membrane hyperpolarization in the presence of Ca
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