Post-translational modifications disclose a dual role for redox stress in cardiovascular pathophysiology

Life Sci. 2015 May 15;129:42-7. doi: 10.1016/j.lfs.2014.11.008. Epub 2014 Nov 27.

Abstract

Although some of the redox changes that occur in biological components may result in deleterious events, this process has recently been tackled as a modulatory event. Advances in our understanding regarding the role of some oxidative/nitrosative reactions revealed that proteins can be structurally and functionally modified by chemical reactions, an epigenetic event known as post-translational modification (PTM). PTMs can function as an "on-off switch" for signaling cascades, and are dependent on the specific generation of redox components such as reactive oxygen species (ROS) and nitric oxide (NO). NO-driven modifications regulate a wide range of cellular processes and have been highlighted as an epigenetic event that protects proteins from proteolytic degradation. On the other hand, ROS-driven modifications are implicated in cell damage in a number of pathological conditions, especially in the cardiovascular system. Therefore, while mitochondrial uncoupling yields the massive production of ROS in the heart, some cellular redox-sensitive pathways trigger PTMs that may play a cardioprotective role. In this review, we present an overview of the oxidative/nitrosative milieu in cardiac pathologies and address the role of the main redox-driven PTMs as epigenetic events in cardioprotection, as well as its regulatory function in cardiomyocyte signaling. Improved understanding of the role of these PTMs in cardiovascular disease can help direct some approaches for future clinical research regarding health risk assessment, as well as inform strategies for disease treatment and prevention.

Keywords: Cardiac disease; Cardioprotection; Oxidative stress; Post-translational modifications.

Publication types

  • Review

MeSH terms

  • Cardiovascular Diseases / physiopathology*
  • Epigenesis, Genetic / physiology*
  • Glycosylation
  • Humans
  • Models, Cardiovascular*
  • Nitric Oxide / metabolism
  • Oxidation-Reduction
  • Oxidative Stress / physiology*
  • Protein Processing, Post-Translational / physiology*
  • Reactive Oxygen Species / metabolism
  • Signal Transduction / physiology*

Substances

  • Reactive Oxygen Species
  • Nitric Oxide