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Review
, 28 (6), 643-657

Autophagy, Cellular Aging and Age-related Human Diseases

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Review

Autophagy, Cellular Aging and Age-related Human Diseases

So Yeong Cheon et al. Exp Neurobiol.

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.

Figures

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.

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