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Liyang MA1*, Tianzhen LIU2*, 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, 1998, -1(-1): .
@article{title="mTOR and lysosome repair: from adaptive response to neurodegenerative vulnerability",
author="Liyang MA1*, Tianzhen LIU2*, Jingyi ZHOU2, Wen TANG2, Jinjie ZHONG2, Ge BAI3, Guoping PENG4, Zhen ZHONG2",
journal="Journal of Zhejiang University Science B",
volume="-1",
number="-1",
pages="",
year="1998",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2500873"
}
%0 Journal Article
%T mTOR and lysosome repair: from adaptive response to neurodegenerative vulnerability
%A Liyang MA1*
%A Tianzhen LIU2*
%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
%V -1
%N -1
%P
%@ 1673-1581
%D 1998
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2500873
TY - JOUR
T1 - mTOR and lysosome repair: from adaptive response to neurodegenerative vulnerability
A1 - Liyang MA1*
A1 - Tianzhen LIU2*
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
VL - -1
IS - -1
SP -
EP -
%@ 1673-1581
Y1 - 1998
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2500873
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.
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