Sep 18, 2013

Role of mitochondrial oxidative stress in hypertension

American Journal of Physiology. Heart and Circulatory Physiology
Sergey Dikalov, Zoltan Ungvari


Based on mosaic theory, hypertension is a multifactorial disorder that develops because of genetic, environmental, anatomical, adaptive neural, endocrine, humoral, and hemodynamic factors. It has been recently proposed that oxidative stress may contribute to all of these factors and production of reactive oxygen species (ROS) play an important role in the development of hypertension. Previous studies focusing on the role of vascular NADPH oxidases provided strong support of this concept. Although mitochondria represent one of the most significant sources of cellular ROS generation, the regulation of mitochondrial ROS generation in the cardiovascular system and its pathophysiological role in hypertension are much less understood. In this review, the role of mitochondrial oxidative stress in the pathophysiology of hypertension and cross talk between angiotensin II signaling, pathways involved in mechanotransduction, NADPH oxidases, and mitochondria-derived ROS are considered. The possible benefits of therapeutic strategies that have the potential to attenuate mitochondrial oxidative stress for the prevention/treatment of hypertension are also discussed.

  • References135
  • Citations57


  • References135
  • Citations57

Mentioned in this Paper

Biochemical Pathway
Cardiovascular System
Blood Vessel
Diastolic Blood Pressure
Antioxidant Effect
Congenital, Hereditary, and Neonatal Diseases and Abnormalities
Mechanotransduction, Cellular
NADPH Oxidase
Oxidative Stress

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