An Overview of Autophagy: Morphology, Mechanism, and Regulation
Open accessAbstract
SIGNIFICANCE: Autophagy is a highly conserved eukaryotic cellular recycling process. Through the degradation of cytoplasmic organelles, proteins, and macromolecules, and the recycling of the breakdown products, autophagy plays important roles in cell survival and maintenance. Accordingly, dysfunction of this process contributes to the pathologies of many human diseases. RECENT ADVANCES: Extensive research is currently being done to better understand the process of autophagy. In this review, we describe current knowledge of the morphology, molecular mechanism, and regulation of mammalian autophagy. CRITICAL ISSUES: At the mechanistic and regulatory levels, there are still many unanswered questions and points of confusion that have yet to be resolved. FUTURE DIRECTIONS: Through further research, a more complete and accurate picture of the molecular mechanism and regulation of autophagy will not only strengthen our understanding of this significant cellular process, but will aid in the development of new treatments for human diseases in which autophagy is not functioning properly.
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Macroautophagy is an evolutionarily conserved eukaryotic pathway for bulk and selective degradation of proteins and organelles.
“Macroautophagy, often referred to simply as autophagy, is an evolutionarily conserved eukaryotic pathway for bulk and selective degradation of proteins and organelles [31].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [31]
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The machinery of macroautophagy
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BackgroundUnravelling the mechanisms regulating muscle mitochondrial biogenesis
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- Authors
- Parzych, K. R., & Klionsky, D. J.
- Affiliations
- University of Michigan (US)
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2014-01-20
- Volume
- 20
- Issue
- 3
- Pages
- 460-473
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- PMC
- PMC3894687
- OpenAlex
- W2089728480
- Cited by
- 2,521
- References
- 163
- Citations by year
- 2026: 160 · 2025: 268 · 2024: 383 · 2023: 350 · 2022: 346 · 2021: 312 · 2020: 262 · 2019: 146 · 2018: 94 · 2017: 61 · 2016: 52 · 2015: 42 · 2014: 35 · 2013: 8
- FWCI
- 5.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Antioxidants and Redox Signaling (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Deep Blue (University of Michigan) (submittedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM053396)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- autophagy, autophagy regulation, autophagy mechanisms, cellular recycling, organelle degradation, autophagy dysfunction, human disease
- MeSH terms
- Animals, Autophagy, Cell Survival, Humans, Pathology
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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