Endothelial mitochondrial dysfunction in hypertension, diabetes, and atherosclerosis

Cardiovascular Research

5 January 2026
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ESC Journals CORONARY ARTERY DISEASE, ACUTE CORONARY SYNDROMES, ACUTE CARDIAC CARE DISEASES OF THE AORTA, PERIPHERAL VASCULAR DISEASE, STROKE Peripheral Vascular and Cerebrovascular Disease HYPERTENSION BASIC SCIENCE

Abstract

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 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.

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