Autophagy in vascular disease. Review uri icon

Overview

MeSH

  • Animals
  • Apoptosis
  • Atherosclerosis
  • Heart Diseases
  • Humans
  • Lung Diseases
  • Lysosomes
  • Phagosomes
  • Reperfusion Injury
  • Signal Transduction
  • Starvation

MeSH Major

  • Autophagy
  • Vascular Diseases

abstract

  • Autophagy, or "self eating," refers to a regulated cellular process for the lysosomal-dependent turnover of organelles and proteins. During starvation or nutrient deficiency, autophagy promotes survival through the replenishment of metabolic precursors derived from the degradation of endogenous cellular components. Autophagy represents a general homeostatic and inducible adaptive response to environmental stress, including endoplasmic reticulum stress, hypoxia, oxidative stress, and exposure to pharmaceuticals and xenobiotics. Whereas elevated autophagy can be observed in dying cells, the functional relationships between autophagy and programmed cell death pathways remain incompletely understood. Preclinical studies have identified autophagy as a process that can be activated during vascular disorders, including ischemia-reperfusion injury of the heart and other organs, cardiomyopathy, myocardial injury, and atherosclerosis. The functional significance of autophagy in human cardiovascular disease pathogenesis remains incompletely understood, and potentially involves both adaptive and maladaptive outcomes, depending on model system. Although relatively few studies have been performed in the lung, our recent studies also implicate a role for autophagy in chronic lung disease. Manipulation of the signaling pathways that regulate autophagy could potentially provide a novel therapeutic strategy in the prevention or treatment of human disease.

publication date

  • February 2010

has subject area

  • Animals
  • Apoptosis
  • Atherosclerosis
  • Autophagy
  • Heart Diseases
  • Humans
  • Lung Diseases
  • Lysosomes
  • Phagosomes
  • Reperfusion Injury
  • Signal Transduction
  • Starvation
  • Vascular Diseases

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC3137148

Digital Object Identifier (DOI)

  • 10.1513/pats.200909-100JS

PubMed ID

  • 20160147

Additional Document Info

start page

  • 40

end page

  • 47

volume

  • 7

number

  • 1