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Autophagy, Cellular Aging and Age-related Human Diseases

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 progress...

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Autores principales: Cheon, So Yeong, Kim, Hyunjeong, Rubinsztein, David C., Lee, Jong Eun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society for Brain and Neural Sciences 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6946111/
https://www.ncbi.nlm.nih.gov/pubmed/31902153
http://dx.doi.org/10.5607/en.2019.28.6.643
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author Cheon, So Yeong
Kim, Hyunjeong
Rubinsztein, David C.
Lee, Jong Eun
author_facet Cheon, So Yeong
Kim, Hyunjeong
Rubinsztein, David C.
Lee, Jong Eun
author_sort Cheon, So Yeong
collection PubMed
description 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.
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spelling pubmed-69461112020-01-15 Autophagy, Cellular Aging and Age-related Human Diseases Cheon, So Yeong Kim, Hyunjeong Rubinsztein, David C. Lee, Jong Eun Exp Neurobiol Review Article 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. The Korean Society for Brain and Neural Sciences 2019-12 2019-12-31 /pmc/articles/PMC6946111/ /pubmed/31902153 http://dx.doi.org/10.5607/en.2019.28.6.643 Text en Copyright © Experimental Neurobiology 2019 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Cheon, So Yeong
Kim, Hyunjeong
Rubinsztein, David C.
Lee, Jong Eun
Autophagy, Cellular Aging and Age-related Human Diseases
title Autophagy, Cellular Aging and Age-related Human Diseases
title_full Autophagy, Cellular Aging and Age-related Human Diseases
title_fullStr Autophagy, Cellular Aging and Age-related Human Diseases
title_full_unstemmed Autophagy, Cellular Aging and Age-related Human Diseases
title_short Autophagy, Cellular Aging and Age-related Human Diseases
title_sort autophagy, cellular aging and age-related human diseases
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6946111/
https://www.ncbi.nlm.nih.gov/pubmed/31902153
http://dx.doi.org/10.5607/en.2019.28.6.643
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