Mitochondrial dysfunction in hypertension: mechanistic pathways and therapeutic implications.

Hypertension is a major global cardiovascular disorder characterized by complex and multifactorial pathogenesis. Although numerous antihypertensive therapies are available, a considerable proportion of patients continue to exhibit inadequate blood pressure control. Emerging evidence underscores the central role of mitochondrial dysfunction in the development and progression of hypertension. As regulators of energy metabolism, redox balance, calcium signaling, and cell survival, mitochondria play a significant role in maintaining vascular and neuronal homeostasis. Mitochondrial abnormalities-such as excessive ROS production, impaired mitophagy, disrupted fusion and fission dynamics, and calcium dysregulation—can amplify vascular dysfunction and sympathetic overactivation, thereby elevating blood pressure. This review summarizes current advances in mitochondrial pathophysiology in hypertension and discusses mitochondrial-targeted therapeutic strategies. Natural products derived from traditional Chinese medicine (e.g., apigenin, berberine, curcumin) and Western compounds (e.g., MitoTEMPO, empagliflozin, Mdivi-1) show promise in mitigating mitochondrial stress and lowering blood pressure. A deeper understanding of mitochondria-centered mechanisms may offer novel opportunities for precision therapy, particularly in resistant hypertension.