4.6 Article

Redox signaling in the cardiomyocyte: From physiology to failure

Journal

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2016.03.002

Keywords

Redox signaling; NADPH oxidase; Heart failure; Reactive oxygen species

Funding

  1. British Heart Foundation
  2. Foundation Leducq Transatlantic Network of Excellence Award
  3. Department of Health via a National Institute for Health Research (NIHR) Biomedical Research Centre
  4. King's College London and King's College Hospital NHS Foundation Trust
  5. British Heart Foundation [RG/13/11/30384] Funding Source: researchfish

Ask authors/readers for more resources

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 O-2 and ROS are major source of electrons in redox reactions in aerobic organisms. Because the heart has the highest O-2 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. (C) 2016 Elsevier Ltd. All rights reserved.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.6
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available