Impact of Chaperone-Mediated Autophagy in Brain Aging: Neurodegenerative Diseases and Glioblastoma

被引：34

作者：

Auzmendi-Iriarte, Jaione ^{[1
]}

Matheu, Ander ^{[1
,2
,3
]}

机构：

[1] Biodonostia Hlth Res Inst, Cellular Oncol Grp, San Sebastian, Spain

[2] CIBER Fragilidad & Envejecimiento Saludable CIBER, Madrid, Spain

[3] Basque Fdn, IKERBASQUE, Bilbao, Spain

来源：

FRONTIERS IN AGING NEUROSCIENCE | 2021年 / 12卷

关键词：

CMA; LAMP2; physiological aging; neurodegenerative diseases; glioblastoma; CENTRAL-NERVOUS-SYSTEM; SURVIVAL FACTOR MEF2D; STEM-CELL ACTIVITY; ALPHA-SYNUCLEIN; RETINOIC ACID; CEREBROSPINAL-FLUID; LYSOSOMAL RECEPTOR; CYTOSOLIC PROTEINS; HIF1A DEGRADATION; INHIBITION;

D O I：

10.3389/fnagi.2020.630743

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

030301 [社会学]; 100201 [内科学];

摘要：

Brain aging is characterized by a time-dependent decline of tissue integrity and function, and it is a major risk for neurodegenerative diseases and brain cancer. Chaperone-mediated autophagy (CMA) is a selective form of autophagy specialized in protein degradation, which is based on the individual translocation of a cargo protein through the lysosomal membrane. Regulation of processes such as proteostasis, cellular energetics, or immune system activity has been associated with CMA, indicating its pivotal role in tissue homeostasis. Since first studies associating Parkinson's disease (PD) to CMA dysfunction, increasing evidence points out that CMA is altered in both physiological and pathological brain aging. In this review article, we summarize the current knowledge regarding the impact of CMA during aging in brain physiopathology, highlighting the role of CMA in neurodegenerative diseases and glioblastoma, the most common and aggressive brain tumor in adults.

引用

页数：17

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