Cited by 6,452Autophagy in Disease and TherapyUbiquitin and proteasome pathwaysCalcium signaling and nucleotide metabolism

Autophagy fights disease through cellular self-digestion

Open access
Mizushima, Noboru, Levine, Beth, Cuervo, Ana Maria, Klionsky, Daniel J.·2008·Nature

Abstract

Autophagy, or cellular self-digestion, is a cellular pathway involved in protein and organelle degradation, with an astonishing number of connections to human disease and physiology. For example, autophagic dysfunction is associated with cancer, neurodegeneration, microbial infection and ageing. Paradoxically, although autophagy is primarily a protective process for the cell, it can also play a role in cell death. Understanding autophagy may ultimately allow scientists and clinicians to harness this process for the purpose of improving human health.

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Crossref · 10.1038/nature06639

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60 of 60 references verified0 citation errors · 0 not checkable

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  • Macroautophagy has a neuroprotective function.

    “The neuroprotective function of macroautophagy has become an interesting focus in neurodegenerative disease, exemplified in Huntington's disease (Menzies et al., 2006;Mizushima et al., 2008), as well as in animal models (Hara et al., 2006;Komatsu et al., 2006).”
  • 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 Mizushima et al., 2008

  • Autophagy has been implicated in establishing the SASP through the TOR autophagy spatial coupling compartment (TASCC).

    “macro-autophagy (hereafter referred to as autophagy)—a tightly regulated major lysosomal degradation pathway (27–30)—has been implicated in establishing the SASP through the target of rapamycin (TOR) autophagy spatial coupling compartment (TASCC).”

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Authors
Mizushima, N., Levine, B., Cuervo, A. M., & Klionsky, D. J.
Affiliations
  • Tokyo Medical and Dental University (JP)
  • The University of Texas at Dallas (US)
  • University of Michigan (US)
Corresponding author
Klionsky, Daniel J.
Venue
Nature
Published
2008-02
Volume
451
Issue
7182
Pages
1069-1075
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
OpenAlex
W1994823455
Cited by
6,452
References
60
Citations by year
2026: 126 · 2025: 233 · 2024: 302 · 2023: 305 · 2022: 361 · 2021: 381 · 2020: 412 · 2019: 392 · 2018: 388 · 2017: 434 · 2016: 439 · 2015: 430 · 2014: 456 · 2013: 400 · 2012: 378
FWCI
35.92
Type
journal article
Language
en
Open access
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
  • Deep Blue (University of Michigan) (submittedVersion)
Funders
  • American Cancer Society
  • Ellison Medical Foundation
  • Ministry of Education, Culture, Sports, Science and Technology
  • Toray Science Foundation
  • National Institutes of Health
  • National Institute on Aging (R03AG019834, R01AG021904, R21AG025355)
  • National Cancer Institute
  • National Institute of General Medical Sciences
  • National Institute of Allergy and Infectious Diseases
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, protein degradation, organelle degradation, cytoprotection, cell death, cancer, neurodegeneration, microbial infection, aging
MeSH terms
Aging, Animals, Autophagy, Cell Survival, Humans, Immunity, Innate, Neoplasms, Cell Death, Neurodegenerative Diseases

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