Redox signaling in pathophysiology of hypertension

J Biomed Sci. 2013 Sep 18;20(1):69. doi: 10.1186/1423-0127-20-69.

Abstract

Reactive oxygen species (ROS) are products of normal cellular metabolism and derive from various sources in different cellular compartments. Oxidative stress resultant from imbalance between ROS generation and antioxidant defense mechanisms is important in pathogenesis of cardiovascular diseases, such as hypertension, heart failure, atherosclerosis, diabetes, and cardiac hypertrophy. In this review we focus on hypertension and address sources of cellular ROS generation, mechanisms involved in regulation of radical homeostasis, superoxide dismutase isoforms in pathophysiology of hypertension; as well as radical intracellular signaling and phosphorylation processes in proteins of the affected cardiovascular tissues. Finally, we discuss the transcriptional factors involved in redox-sensitive gene transcription and antioxidant response, as well as their roles in hypertension.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cardiovascular System / metabolism
  • Cardiovascular System / physiopathology*
  • Humans
  • Hypertension / etiology
  • Hypertension / physiopathology*
  • Mice
  • Oxidation-Reduction
  • Rats
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction

Substances

  • Reactive Oxygen Species