Autophagy as a pro-death pathway

Immunol Cell Biol. 2015 Jan;93(1):35-42. doi: 10.1038/icb.2014.85. Epub 2014 Oct 21.

Abstract

The evolutionarily conserved catabolic process of autophagy involves the degradation of cytoplasmic components through lysosomal enzymes. Basal levels of autophagy maintain cellular homeostasis and under stress conditions high levels of autophagy are induced. It is often under such stress conditions that high levels of autophagy and cell death have been observed, leading to the idea that autophagy may act as an executioner of cell death. However the notion of autophagy as a cell death mechanism has been controversial and remains mechanistically undefined. There is now growing evidence that in specific contexts autophagy can indeed facilitate cell death. The pro-death role of autophagy is however complicated due to the extensive cross-talk between different signalling pathways. This review summarises the examples of where autophagy acts as a means of cell death and discusses the association of autophagy with the different cell death pathways.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Apoptosis / immunology
  • Autophagy / genetics*
  • Autophagy / immunology
  • Caenorhabditis elegans / genetics
  • Caenorhabditis elegans / immunology
  • Dictyostelium / genetics
  • Dictyostelium / immunology
  • Drosophila melanogaster / genetics
  • Drosophila melanogaster / immunology
  • Gene Expression Regulation
  • Humans
  • Immunity, Innate
  • Lysosomes / genetics
  • Lysosomes / immunology
  • Neoplasm Proteins / genetics*
  • Neoplasm Proteins / immunology
  • Neoplasms / genetics*
  • Neoplasms / immunology
  • Neoplasms / pathology
  • Phagosomes / genetics*
  • Phagosomes / immunology
  • Signal Transduction
  • Stress, Physiological
  • Ubiquitin-Conjugating Enzymes / genetics*
  • Ubiquitin-Conjugating Enzymes / immunology

Substances

  • Neoplasm Proteins
  • Ubiquitin-Conjugating Enzymes