衰老相关的蛋白稳态失衡

doi:10.16288/j.yczz.22-126

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Hereditas(Beijing) ›› 2022, Vol. 44 ›› Issue (9): 733-744.doi: 10.16288/j.yczz.22-126

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Age-associated proteostasis collapse

Jiali Li(), Jin Li(), Hu Wang()

Key Laboratory of Ageing and Cancer Biology of Zhejiang Province, Institute of Ageing Research, Hangzhou Normal Universtiy School of Medicine, Hangzhou 311121, China

Received:2022-04-26 Revised:2022-06-28 Online:2022-09-20 Published:2022-07-27
Contact: Li Jin,Wang Hu E-mail:lijiali_carry@163.com;lijin@hznu.edu.cn;20120066@hznu.edu.cn
Supported by:
Supported by the National Key Research and Development Program of China Nos(2018YFA0109300);Supported by the National Key Research and Development Program of China Nos(2021YFA1102800);the National Natural Science Fund for Excellent Young Scholars No(82022026);the Science Foundation for Distinguished Young Scholars of Guangdong Province No(2019B151502008);the Natural Science Foundation of Zhejiang Province No(LQ22H250001)

Abstract

Abstract:

Healthy cells utilize a series of protein quality regulatory networks to maintain the integrity and functionality of their proteome, named as protein homeostasis (proteostasis). However, the phenomenon of proteostasis collapse, including the destruction of the balance between protein synthesis, folding and degradation, are common with aging. The main causes of age-associated proteostasis collapse are as follows: (1) the decline in transcriptional activation of stress response related pathways, (2) the reduction of proteasome and autophagy activity, and (3) ribosome pausing during translation. In addition, proteostasis is regulated mainly through chaperones, proteasomes, and autophagy systems of proteostasis network in aging. This paper mainly reviews the causes of age-associated proteostasis collapse and the pathways of proteostasis regulation, which may open the way to explore aging studies and solve aging problems.

Key words: aging, proteostasis collapse, proteostasis network

Jiali Li, Jin Li, Hu Wang. Age-associated proteostasis collapse[J]. Hereditas(Beijing), 2022, 44(9): 733-744.

Figures/Tables 2

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