Regulation mechanisms and signaling pathways of autophagy
Open accessAbstract
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.
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Three different forms of autophagy have been described in mammalian cells: macroautophagy, microautophagy and chaperone-mediated autophagy.
“Three different forms of autophagy have been described in mammalian cells: macroautophagy, microautophagy and chaperone-mediated autophagy (Fig. 3) (Cuervo, 2009; He and Klionsky, 2009; Mizushima et al., 2008).”
From Protein Homeostasis and Aging: the importance of exquisite quality control (2011) · cites this paper as He and Klionsky, 2009
The Introduction (page unavailable) describes autophagosomes in mammalian cells, supporting the macroautophagy portion of the claim. Our copy does not identify microautophagy or chaperone-mediated autophagy as the other two forms, or state the three-part classification (searched both terms and the three-form phrasing). (LLM, conf=0.84)
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- Authors
- He, C., & Klionsky, D. J.
- Affiliations
- University of Michigan (US)
- Venue
- Annual Review of Genetics
- Publisher
- Annual Reviews
- Published
- 2009-12-01
- Volume
- 43
- Issue
- 1
- Pages
- 67-93
- ISSN
- 0066-4197 (ISSN-L)
- 1545-2948
- PMC
- PMC2831538
- OpenAlex
- W2096308078
- Cited by
- 3,609
- References
- 20
- Citations by year
- 2026: 89 · 2025: 117 · 2024: 184 · 2023: 188 · 2022: 198 · 2021: 258 · 2020: 270 · 2019: 253 · 2018: 276 · 2017: 291 · 2016: 249 · 2015: 246 · 2014: 251 · 2013: 199 · 2012: 229
- FWCI
- 21.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Genetics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (GM 53396, R01GM053396)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- autophagy, autophagy regulation, signaling pathways, autophagy machinery, stress response, starvation, endoplasmic reticulum stress, growth factor deprivation, pathogen infection, lysosomal degradation, transcriptional activation, post-translational modification, cancer, neurodegeneration, infectious diseases
- MeSH terms
- Animals, Autophagy, Eukaryotic Cells, Gene Expression Regulation, Humans, Lysosomes, Phagosomes, Signal Transduction
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