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Cited by 3,802

The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.

Autophagy: cellular and molecular mechanisms

Open access
Glick, Danielle, Barth, Sandra, Macleod, Kay F.·2010·The Journal of Pathology
DOI 10.1002/path.2697
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Abstract

Autophagy is a self‐degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress. Autophagy also plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria, endoplasmic reticulum and peroxisomes, as well as eliminating intracellular pathogens. Thus, autophagy is generally thought of as a survival mechanism, although its deregulation has been linked to non‐apoptotic cell death. Autophagy can be either non‐selective or selective in the removal of specific organelles, ribosomes and protein aggregates, although the mechanisms regulating aspects of selective autophagy are not fully worked out. In addition to elimination of intracellular aggregates and damaged organelles, autophagy promotes cellular senescence and cell surface antigen presentation, protects against genome instability and prevents necrosis, giving it a key role in preventing diseases such as cancer, neurodegeneration, cardiomyopathy, diabetes, liver disease, autoimmune diseases and infections. This review summarizes the most up‐to‐date findings on how autophagy is executed and regulated at the molecular level and how its disruption can lead to disease. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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Citations

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1 retracted

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Metadata

Authors
Glick, D., Barth, S., & Macleod, K. F.
Venue
The Journal of Pathology
Publisher
Wiley
Published
2010-04
Volume
221
Issue
1
Pages
3-12
ISSN
  • 0022-3417 (ISSN-L)
  • 1096-9896
DOI
10.1002/path.2697
OpenAlex
W2159754384
Cited by
3,802
References
27
FWCI
45.50
Type
journal article
Language
en
Open access
green
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.