Redox signaling in the cardiomyocyte: From physiology to failure

Int J Biochem Cell Biol. 2016 May:74:145-51. doi: 10.1016/j.biocel.2016.03.002. Epub 2016 Mar 14.

Abstract

The specific effect of oxygen and reactive oxygen species (ROS) in mediating post-translational modification of protein targets has emerged as a key mechanism regulating signaling components, a process termed redox signaling. ROS act in the post-translational modification of multiple target proteins including receptors, kinases, phosphatases, ion channels and transcription factors. Both O2 and ROS are major source of electrons in redox reactions in aerobic organisms. Because the heart has the highest O2 consumption among body organs, it is not surprising that redox signaling is central to heart function and pathophysiology. In this article, we review some of the main cardiac redox signaling pathways and their roles in the cardiomyocyte and in heart failure, with particular focus on the specific molecular targets of ROS in the heart.

Keywords: Heart failure; NADPH oxidase; Reactive oxygen species; Redox signaling.

Publication types

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

MeSH terms

  • Heart Failure / physiopathology
  • Humans
  • Myocytes, Cardiac / pathology
  • Myocytes, Cardiac / physiology*
  • Oxidation-Reduction*
  • Protein Processing, Post-Translational
  • Reactive Oxygen Species
  • Signal Transduction

Substances

  • Reactive Oxygen Species