Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 28 (6), 643-657

Autophagy, Cellular Aging and Age-related Human Diseases


Autophagy, Cellular Aging and Age-related Human Diseases

So Yeong Cheon et al. Exp Neurobiol.


Macroautophagy/autophagy is a conserved degradation system that engulfs intracytoplasmic contents, including aggregated proteins and organelles, which is crucial for cellular homeostasis. During aging, cellular factors suggested as the cause of aging have been reported to be associated with progressively compromised autophagy. Dysfunctional autophagy may contribute to age-related diseases, such as neurodegenerative disease, cancer, and metabolic syndrome, in the elderly. Therefore, restoration of impaired autophagy to normal may help to prevent age-related disease and extend lifespan and longevity. Therefore, this review aims to provide an overview of the mechanisms of autophagy underlying cellular aging and the consequent disease. Understanding the mechanisms of autophagy may provide potential information to aid therapeutic interventions in age-related diseases.

Keywords: Aging; Autophagy; DNA damage; Oxidative stress; SASP; Telomere shortening.


Fig. 1
Fig. 1
Schematic overview of the autophagy process. Initially, a precursor form of the autophagosome, a phagophore is formed by various sources including ER, Golgi, mitochondria, endosomes, and plasma membrane. This cup-shaped and double membrane structure extends its edges to form an autophagosome. Closed autophagosomes containing engulfed cytoplasmic proteins or organelles migrate toward the perinuclear part of the cells where lysosomes are clustered to enable autophagosome-lysosome fusion. Alternatively, autophagosomes can generate amphisomes by fusion with endosomes. Ultimately, autophagosomes or amphisomes fuse with lysosomes where their contents are degraded.

Similar articles

  • Autophagy and the Cell Biology of Age-Related Disease
    AM Leidal et al. Nat Cell Biol 20 (12), 1338-1348. PMID 30482941. - Review
    Macroautophagy (autophagy) is a conserved lysosomal degradation process essential for cellular homeostasis and adaption to stress. Accumulating evidence indicates that au …
  • Autophagy, Aging, and Longevity
    L Luo et al. Adv Exp Med Biol 1206, 509-525. PMID 31777001. - Review
    Autophagy is a conserved process that degrades intracellular components through lysosomes, thereby maintaining energy homeostasis and renewal of organelles. Mounting evid …
  • Mitophagy, Mitochondrial Dynamics, and Homeostasis in Cardiovascular Aging
    NN Wu et al. Oxid Med Cell Longev 2019, 9825061. PMID 31781358. - Review
    Biological aging is an inevitable and independent risk factor for a wide array of chronic diseases including cardiovascular and metabolic diseases. Ample evidence has est …
  • Staying Young at Heart: Autophagy and Adaptation to Cardiac Aging
    LJ Leon et al. J Mol Cell Cardiol 95, 78-85. PMID 26549356. - Review
    Aging is a predominant risk factor for developing cardiovascular disease. Therefore, the cellular processes that contribute to aging are attractive targets for therapeuti …
  • Astrocytes Autophagy in Aging and Neurodegenerative Disorders
    JL Wang et al. Biomed Pharmacother 122, 109691. PMID 31786465. - Review
    Astrocytes can serve multiple functions in maintaining cellular homeostasis of the central nervous system (CNS), and normal functions for autophagy in astrocytes is consi …
See all similar articles


    1. Rubinsztein DC, Mariño G, Kroemer G. Autophagy and aging. Cell. 2011;146:682–695. doi: 10.1016/j.cell.2011.07.030. - DOI - PubMed
    1. Hansen M, Rubinsztein DC, Walker DW. Autophagy as a promoter of longevity: insights from model organisms. Nat Rev Mol Cell Biol. 2018;19:579–593. doi: 10.1038/s41580-018-0033-y. - DOI - PMC - PubMed
    1. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell. 2013;153:1194–1217. doi: 10.1016/j.cell.2013.05.039. - DOI - PMC - PubMed
    1. Balaban RS, Nemoto S, Finkel T. Mitochondria, oxidants, and aging. Cell. 2005;120:483–495. doi: 10.1016/j.cell.2005.02.001. - DOI - PubMed
    1. Seluanov A, Mittelman D, Pereira-Smith OM, Wilson JH, Gorbunova V. DNA end joining becomes less efficient and more error-prone during cellular senescence. Proc Natl Acad Sci U S A. 2004;101:7624–7629. doi: 10.1073/pnas.0400726101. - DOI - PMC - PubMed