mTORC1 Crosstalk With Stress Granules in Aging and Age-Related Diseases

被引：12

作者：

Cadena Sandoval, Marti ^{[1
,2
,3
]}

Heberle, Alexander Martin ^{[1
,2
,3
]}

Rehbein, Ulrike ^{[1
,2
]}

Barile, Cecilia ^{[1
,2
]}

Ramos Pittol, Jose Miguel ^{[1
,2
]}

Thedieck, Kathrin ^{[1
,2
,3
,4
]}

机构：

[1] Univ Innsbruck, Inst Biochem, Innsbruck, Austria

[2] Univ Innsbruck, Ctr Mol Biosci Innsbruck, Innsbruck, Austria

[3] Univ Med Ctr Groningen, Univ Groningen, Sect Syst Med Metab & Signaling, Lab Pediat, Groningen, Netherlands

[4] Carl von Ossietzky Univ Oldenburg, Sch Med & Hlth Sci, Dept Neurosci, Oldenburg, Germany

来源：

FRONTIERS IN AGING | 2021年 / 2卷

关键词：

MTOR; aging hallmarks; stress; insulin; amino acids; cellular signaling; stress granules (SGs); autophagy; ENDOPLASMIC-RETICULUM STRESS; RAPAMYCIN COMPLEX 1; RNA-BINDING PROTEINS; CELL-CYCLE ARREST; P70; S6; KINASE; AMINO-ACID; TUBEROUS SCLEROSIS; RAG GTPASES; TRANSLATION INITIATION; MAMMALIAN TARGET;

D O I：

10.3389/fragi.2021.761333

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

The mechanistic target of rapamycin complex 1 (mTORC1) kinase is a master regulator of metabolism and aging. A complex signaling network converges on mTORC1 and integrates growth factor, nutrient and stress signals. Aging is a dynamic process characterized by declining cellular survival, renewal, and fertility. Stressors elicited by aging hallmarks such as mitochondrial malfunction, loss of proteostasis, genomic instability and telomere shortening impinge on mTORC1 thereby contributing to age-related processes. Stress granules (SGs) constitute a cytoplasmic non-membranous compartment formed by RNA-protein aggregates, which control RNA metabolism, signaling, and survival under stress. Increasing evidence reveals complex crosstalk between the mTORC1 network and SGs. In this review, we cover stressors elicited by aging hallmarks that impinge on mTORC1 and SGs. We discuss their interplay, and we highlight possible links in the context of aging and age-related diseases.

引用

页数：13

共 210 条

[11] Translocation of PDK-1 to the plasma membrane is important in allowing PDK-1 to activate protein kinase B [J].