Relationships between protein degradation, cellular senescence, and organismal aging.

aging autophagy proteasome proteostasis senescence

Journal

Journal of biochemistry
ISSN: 1756-2651
Titre abrégé: J Biochem
Pays: England
ID NLM: 0376600

Informations de publication

Date de publication:
13 Feb 2024
Historique:
received: 07 01 2024
revised: 01 02 2024
accepted: 07 02 2024
medline: 13 2 2024
pubmed: 13 2 2024
entrez: 13 2 2024
Statut: aheadofprint

Résumé

Aging is a major risk factor for many diseases. Recent studies have shown that age-related disruption of proteostasis leads to the accumulation of abnormal proteins and that dysfunction of the two major intracellular proteolytic pathways, the ubiquitin-proteasome pathway, and the autophagy-lysosome pathway, is largely responsible for this process. Conversely, it has been shown that activation of these proteolytic pathways may contribute to lifespan extension and suppression of pathological conditions, making it a promising intervention for anti-aging. This review provides an overview of the important role of intracellular protein degradation in aging and summarizes how the disruption of proteostasis is involved in age-related diseases.

Identifiants

pubmed: 38348509
pii: 7606910
doi: 10.1093/jb/mvae016
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© The Author(s) 2024. Published by Oxford University Press on behalf of the Japanese Biochemical Society.

Auteurs

Jun Hamazaki (J)

Laboratory of Protein Metabolism, Graduate School of Pharmaceutical Sciences, the University of Tokyo, Bunkyo-ku, Tokyo 1130033, Japan.

Shigeo Murata (S)

Laboratory of Protein Metabolism, Graduate School of Pharmaceutical Sciences, the University of Tokyo, Bunkyo-ku, Tokyo 1130033, Japan.

Classifications MeSH