Autophagy: Basic Principles and Relevance to Disease

Kundu, Mondira; Thompson, Craig B.

doi:10.1146/annurev.pathmechdis.2.010506.091842

Cited by 523Autophagy in Disease and TherapyCalcium signaling and nucleotide metabolismUbiquitin and proteasome pathways

Autophagy: Basic Principles and Relevance to Disease

Kundu, Mondira, Thompson, Craig B.·2008·Annual Review of Pathology: Mechanisms of Disease

DOI 10.1146/annurev.pathmechdis.2.010506.091842

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Abstract

Autophagy is a process by which cytoplasmic components are sequestered in double membrane vesicles and degraded upon fusion with lysosomal compartments. In yeast, autophagy is activated in response to changes in the extracellular milieu. Depending upon the stimulus, autophagy can degrade cytoplasmic contents nonspecifically or can target the degradation of specific cellular components. Both of these have been adopted in higher eukaryotes and account for the expanding role of autophagy in various cellular processes, as well as contribute to the variation in cellular outcomes after induction of autophagy. In some cases, autophagy appears to be an adaptive response, whereas under other circumstances it is involved in cell death. In mammals, autophagy has been implicated in either the pathogenesis or response to a wide variety of diseases, including neurodegenerative disease, chronic bacterial and viral infections, atherosclerosis, and cancer. As the basic molecular pathways that regulate autophagy are elucidated, the relationship of autophagy to the pathogenesis of various disease states emerges.

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AMPK activation and mTOR inhibition are potent activators of autophagy.
“AMPK activation and mTOR inhibition are also both potent activators of autophagy, a catabolic process induced during starvation that promotes the degradation and recycling of cellular components [reviewed in detail in (24)].”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [24]

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Authors: Kundu, M., & Thompson, C. B.
Affiliations: University of Pennsylvania (US)
ORCID: Kundu, Mondira
Thompson, Craig B.
Venue: Annual Review of Pathology: Mechanisms of Disease
Publisher: Annual Reviews
Published: 2008-02-01
Volume: 3
Issue: 1
Pages: 427-455
ISSN: 1553-4006 (ISSN-L)
1553-4014
DOI: 10.1146/annurev.pathmechdis.2.010506.091842
OpenAlex: W2157045574
Cited by: 523
References: 129
Citations by year: 2026: 7 · 2025: 5 · 2024: 9 · 2023: 21 · 2022: 14 · 2021: 20 · 2020: 28 · 2019: 29 · 2018: 37 · 2017: 34 · 2016: 27 · 2015: 32 · 2014: 31 · 2013: 49 · 2012: 47
FWCI: 4.75
Type: journal article
Language: en
Open access: closed
Locations: Annual Review of Pathology Mechanisms of Disease (publishedVersion)
PubMed (publishedVersion)
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, lysosomal degradation, double-membrane vesicles, selective autophagy, autophagy regulation, neurodegenerative diseases, chronic bacterial infection, viral infection, atherosclerosis, cancer, pathogenesis
MeSH terms: Animals, Autophagy, Disease, Humans, Lysosomes

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