Endothelial mitochondrial dysfunction in hypertension, diabetes and atherosclerosis

Abstract 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 signalling molecules, modulate metabolic pathways, and control cell survival. Mitochondrial dysfunction is characterised by excessive reactive oxygen species production, loss of membrane potential, calcium leakage, and structural abnormalities, 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.