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Mitochondria are essential organelles that generate adenosine triphosphate during oxidative phosphorylation by the electron transport chain. Beyond energy production, mitochondria regulate intracellular calcium homeostasis, generate signaling molecules, modulate metabolic pathways, and control cell survival. Mitochondrial dysfunction is characterized by excessive reactive oxygen species production, loss of membrane potential, calcium leakage, and structural abnormalities, which ultimately lead to cell death. In endothelial cells, mitochondrial dysfunction drives endothelial impairment and contributes to cardiovascular diseases. This review explores the mechanisms underlying endothelial mitochondrial dysfunction and examines its role in the development and progression of hypertension, atherosclerosis, and diabetes.
Singh et al. (Thu,) studied this question.