Cited by 424Autophagy in Disease and TherapyGenetics, Aging, and Longevity in Model OrganismsCalcium signaling and nucleotide metabolism

Autophagy and the cell biology of age-related disease

Leidal, Andrew M., Levine, Beth, Debnath, Jayanta·2018·Nature Cell Biology

Abstract

Macroautophagy (autophagy) is a conserved lysosomal degradation process essential for cellular homeostasis and adaption to stress. Accumulating evidence indicates that autophagy declines with age and that impaired autophagy predisposes individuals to age-related diseases, whereas interventions that stimulate autophagy often promote longevity. In this Review, we examine how the autophagy pathway restricts cellular damage and degeneration, and the impact of these functions towards tissue health and organismal lifespan.

Integrity signals

Registry

Crossref · 10.1038/s41556-018-0235-8

Cites

151 of 151 references verified0 citation errors · 0 not checkable

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Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Autophagy is inhibited in aging cells.

    “Autophagy is inhibited in aging cells.”
  • Autophagy capacity decreases with age.

    “Autophagy capacity decreases with age.”
  • Fusion of autophagosomes with lysosomes requires microtubule-based transport, tethering factors, and SNARE proteins.

    “Fusion of autophagosomes with lysosomes requires microtubule-based transport, tethering factors, and SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein [SNAP] receptor) proteins (Leidal et al., 2018; Levine and Kroemer, 2019).”

    From The cell biology of the retinal pigment epithelium (2020) · cites this paper as Leidal et al., 2018

  • In autophagy, damaged organelles and cellular material are enclosed in a double-membraned autophagosome and delivered to lysosomes for degradation.

    “In autophagy, damaged organelles (e.g., mitochondria, lysosomes, peroxisomes) and cellular material (e.g., proteins, lipids, nucleic acids) are enclosed in a double-membraned autophagosome and delivered to lysosomes for degradation (Leidal et al., 2018; Levine and Kroemer, 2019).”

    From The cell biology of the retinal pigment epithelium (2020) · cites this paper as Leidal et al., 2018

  • Prolonged stress downregulates autophagy, which could send the cell into a spiral of increased debris, mitochondrial injury, and eventual metabolic reprogramming.

    “However, prolonged stress downregulates autophagy, which could send the cell into a spiral of increased debris, mitochondrial injury, and eventual metabolic reprogramming (Leidal et al., 2018; Levine and Kroemer, 2019).”

    From The cell biology of the retinal pigment epithelium (2020) · cites this paper as Leidal et al., 2018

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Authors
Leidal, A. M., Levine, B., & Debnath, J.
Affiliations
  • University of California, San Francisco (US)
  • Howard Hughes Medical Institute (US)
Corresponding author
Debnath, Jayanta
Venue
Nature Cell Biology
Published
2018-11-26
Volume
20
Issue
12
Pages
1338-1348
ISSN
  • 1465-7392 (ISSN-L)
  • 1476-4679
OpenAlex
W2900968153
Cited by
424
References
151
Citations by year
2026: 27 · 2025: 62 · 2024: 52 · 2023: 53 · 2022: 58 · 2021: 68 · 2020: 65 · 2019: 39
FWCI
6.41
Type
journal article
Language
en
Open access
closed
Locations
  • Nature Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
Keywords
autophagy, macroautophagy, aging, age-related diseases, longevity, lysosomal degradation, cellular homeostasis, cell damage, autophagy modulators, lifespan
MeSH terms
Aging, Animals, Autophagy, Humans, Lysosomes, Models, Biological, Cardiomyopathies, Signal Transduction, Cellular Senescence, Neurodegenerative Diseases

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