Regulation mechanisms and signaling pathways of autophagy

Congcong He, Daniel J. Klionsky

Research output: Contribution to journalReview articlepeer-review

2927 Scopus citations


Autophagy is a process of self-degradation of cellular components in which double-membrane autophagosomes sequester organelles or portions of cytosol and fuse with lysosomes or vacuoles for breakdown by resident hydrolases. Autophagy is upregulated in response to extra-or intracellular stress and signals such as starvation, growth factor deprivation, ER stress, and pathogen infection. Defective autophagy plays a significant role in human pathologies, including cancer, neurodegeneration, and infectious diseases. We present our current knowledge on the key genes composing the autophagy machinery in eukaryotes from yeast to mammalian cells and the signaling pathways that sense the status of different types of stress and induce autophagy for cell survival and homeostasis. We also review the recent advances on the molecular mechanisms that regulate the autophagy machinery at various levels, from transcriptional activation to post-translational protein modification.

Original languageEnglish (US)
Pages (from-to)67-93
Number of pages27
JournalAnnual review of genetics
StatePublished - Dec 1 2009


  • Atg proteins
  • Lysosome
  • Pathogen
  • Stress
  • Target of rapamycin
  • Transcription

ASJC Scopus subject areas

  • Genetics


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