Autophagy as a regulator of cardiovascular redox homeostasis

Free Radic Biol Med. 2017 Aug:109:108-113. doi: 10.1016/j.freeradbiomed.2016.12.003. Epub 2016 Dec 7.

Abstract

Autophagy is a highly regulated process involving the removal of damaged proteins and organelles from cells and tissues through a lysosomal-mediated pathway. Accumulating evidence suggests that autophagy is necessary to maintain redox homeostasis. Here, we explore the connection between autophagy and reactive oxygen species (ROS). In particular, we discuss how oxidant-dependent signaling can modulate autophagic flux and how autophagy can, in turn, modulate ROS levels. Finally, we discuss how a decline or disruption of autophagy might contribute to redox-dependent cardiovascular pathology and help fuel the age-dependent decline in cardiovascular function.

Keywords: Autophagy; Cardiovascular disease; Mitophagy; ROS.

Publication types

  • Review

MeSH terms

  • Animals
  • Autophagy / genetics*
  • Autophagy-Related Proteins / genetics
  • Autophagy-Related Proteins / metabolism
  • Cardiovascular Diseases / genetics
  • Cardiovascular Diseases / metabolism*
  • Cardiovascular Diseases / pathology
  • Cardiovascular System / metabolism
  • Cardiovascular System / pathology
  • Cysteine Endopeptidases / genetics
  • Cysteine Endopeptidases / metabolism
  • Endothelial Cells / metabolism*
  • Endothelial Cells / pathology
  • Gene Expression Regulation
  • Homeostasis / genetics
  • Humans
  • Lysosomes / metabolism
  • Mitochondria / metabolism*
  • Mitochondria / pathology
  • Mitophagy / genetics
  • Oxidation-Reduction
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction
  • Transient Receptor Potential Channels / genetics
  • Transient Receptor Potential Channels / metabolism

Substances

  • Autophagy-Related Proteins
  • MCOLN1 protein, human
  • Reactive Oxygen Species
  • Transient Receptor Potential Channels
  • ATG4A protein, human
  • Cysteine Endopeptidases