JZUS - Journal of Zhejiang University SCIENCE

Journal of Zhejiang University SCIENCE B

Accepted manuscript available online (unedited version)

mTOR and lysosome repair: from adaptive response to neurodegenerative vulnerability

Author(s): Liyang MA^1, Tianzhen LIU^2, Jingyi ZHOU², Wen TANG², Jinjie ZHONG², Ge BAI³, Guoping PENG⁴, Zhen ZHONG²
Affiliation(s): ¹Chu Kochen Honors College; more
Corresponding email(s): Guoping PENG, email: Guopingpeng@zju.edu.cn Zhen ZHONG, email: zhenzhong@zju.edu.cn
Key Words: mTOR; Lysosomes; Lysosomal damage response; Neurodegenerative diseases

Share this article to： More <<< Previous Paper \|Next Paper >>>

Liyang MA^1*, Tianzhen LIU^2*, Jingyi ZHOU², Wen TANG², Jinjie ZHONG², Ge BAI³, Guoping PENG⁴, Zhen ZHONG². mTOR and lysosome repair: from adaptive response to neurodegenerative vulnerability[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org/10.1631/jzus.B2500873

@article{title="mTOR and lysosome repair: from adaptive response to neurodegenerative vulnerability",
author="Liyang MA^1*, Tianzhen LIU^2*, Jingyi ZHOU², Wen TANG², Jinjie ZHONG², Ge BAI³, Guoping PENG⁴, Zhen ZHONG²",
journal="Journal of Zhejiang University Science B",
year="in press",
publisher="Zhejiang University Press & Springer",
doi="https://doi.org/10.1631/jzus.B2500873"
}

%0 Journal Article
%T mTOR and lysosome repair: from adaptive response to neurodegenerative vulnerability
%A Liyang MA^1*
%A Tianzhen LIU^2*
%A Jingyi ZHOU²
%A Wen TANG²
%A Jinjie ZHONG²
%A Ge BAI³
%A Guoping PENG⁴
%A Zhen ZHONG²
%J Journal of Zhejiang University SCIENCE B
%P
%@ 1673-1581
%D in press
%I Zhejiang University Press & Springer
doi="https://doi.org/10.1631/jzus.B2500873"

TY - JOUR
T1 - mTOR and lysosome repair: from adaptive response to neurodegenerative vulnerability
A1 - Liyang MA^1*
A1 - Tianzhen LIU^2*
A1 - Jingyi ZHOU²
A1 - Wen TANG²
A1 - Jinjie ZHONG²
A1 - Ge BAI³
A1 - Guoping PENG⁴
A1 - Zhen ZHONG²
J0 - Journal of Zhejiang University Science B
SP -
EP -
%@ 1673-1581
Y1 - in press
PB - Zhejiang University Press & Springer
ER -
doi="https://doi.org/10.1631/jzus.B2500873"

Abstract
Chinese Summary
Academic Network
Reviewer Comment

Abstract: Dysregulation of mechanistic target of rapamycin (mTOR) signaling is a common feature of neurodegenerative disease, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), frontotemporal dementia (FTD), and amyotrophic lateral sclerosis (ALS). Under physiological conditions, transient lysosomal rupture triggers a protective response: mTOR activity is temporarily suppressed, autophagy is activated, and lysosomal repair programs re-establish cellular homeostasis. However, chronic mTOR hyperactivation-driven by genetic variants, aging-related signaling changes, or metabolic imbalance-can impair this adaptive lysosomal stress response. Persistent mTOR activity impairs lysosomal repair efficiency and autophagic clearance, promoting the accumulation of damaged organelles and protein aggregates. Building on this compromised degradative capacity, mTOR dysregulation may not directly initiate disease, but instead sensitizes cells to proteotoxic and lysosomal stress, markedly increasing vulnerability. This review integrates findings that support mTOR-associated lysosomal vulnerability as a convergent mechanism in post-mitotic cells and discusses its implications for cellular resilience, disease susceptibility, and therapeutic intervention.

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

Open peer comments: Debate/Discuss/Question/Opinion

<1>

- Go to

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference