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Exp Neurobiol. 2019 Dec 31;28(6):643-657. doi: 10.5607/en.2019.28.6.643.

Autophagy, Cellular Aging and Age-related Human Diseases.

Experimental neurobiology

So Yeong Cheon, Hyunjeong Kim, David C Rubinsztein, Jong Eun Lee

Affiliations

  1. Department of Medical Genetics, Cambridge Institute for Medical Research (CIMR), University of Cambridge, Cambridge CB2 0XY, United Kingdom.
  2. Department of Anatomy, Yonsei University College of Medicine, Seoul 03722, Korea.
  3. UK Dementia Research Institute, University of Cambridge, Cambridge CB2 0AH, United Kingdom.
  4. BK21 PLUS Project for Medical Science, and Brain Research Institute, Yonsei University College of Medicine, Seoul 03722, Korea.

PMID: 31902153 PMCID: PMC6946111 DOI: 10.5607/en.2019.28.6.643

Abstract

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

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