Autophagy in vascular disease

Stefan W. Ryter, Seon Jin Lee, Akaya Smith, Augustine M.K. Choi

Research output: Contribution to journalReview article

71 Scopus citations

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 inhumancardiovascular disease pathogenesis remains incompletely understood, andpotentially involves both adaptiveandmaladaptive 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.

Original languageEnglish (US)
Pages (from-to)40-47
Number of pages8
JournalProceedings of the American Thoracic Society
Volume7
Issue number1
DOIs
StatePublished - Feb 15 2010

Keywords

  • Apoptosis
  • Autophagy
  • Vascular disease

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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