PMID- 35406769
OWN - NLM
STAT- MEDLINE
DCOM- 20220413
LR  - 20220517
IS  - 2073-4409 (Electronic)
IS  - 2073-4409 (Linking)
VI  - 11
IP  - 7
DP  - 2022 Apr 2
TI  - Chaperone-Mediated Autophagy in Neurodegenerative Diseases and Acute Neurological 
      Insults in the Central Nervous System.
LID - 10.3390/cells11071205 [doi]
LID - 1205
AB  - Autophagy is an important function that mediates the degradation of intracellular 
      proteins and organelles. Chaperone-mediated autophagy (CMA) degrades selected 
      proteins and has a crucial role in cellular proteostasis under various 
      physiological and pathological conditions. CMA dysfunction leads to the 
      accumulation of toxic protein aggregates in the central nervous system (CNS) and 
      is involved in the pathogenic process of neurodegenerative diseases, including 
      Parkinson's disease and Alzheimer's disease. Previous studies have suggested that 
      the activation of CMA to degrade aberrant proteins can provide a neuroprotective 
      effect in the CNS. Recent studies have shown that CMA activity is upregulated in 
      damaged neural tissue following acute neurological insults, such as cerebral 
      infarction, traumatic brain injury, and spinal cord injury. It has been also 
      suggested that various protein degradation mechanisms are important for removing 
      toxic aberrant proteins associated with secondary damage after acute neurological 
      insults in the CNS. Therefore, enhancing the CMA pathway may induce 
      neuroprotective effects not only in neurogenerative diseases but also in acute 
      neurological insults. We herein review current knowledge concerning the 
      biological mechanisms involved in CMA and highlight the role of CMA in 
      neurodegenerative diseases and acute neurological insults. We also discuss the 
      possibility of developing CMA-targeted therapeutic strategies for effective 
      treatments.
FAU - Kanno, Haruo
AU  - Kanno H
AUID- ORCID: 0000-0003-1985-2257
AD  - Department of Orthopaedic Surgery, Tohoku Medical and Pharmaceutical University, 
      Sendai 983-8536, Japan.
AD  - Department of Orthopaedic Surgery, Tohoku University School of Medicine, Sendai 
      980-8574, Japan.
FAU - Handa, Kyoichi
AU  - Handa K
AD  - Department of Orthopaedic Surgery, Tohoku University School of Medicine, Sendai 
      980-8574, Japan.
FAU - Murakami, Taishi
AU  - Murakami T
AD  - Department of Orthopaedic Surgery, Tohoku University School of Medicine, Sendai 
      980-8574, Japan.
FAU - Aizawa, Toshimi
AU  - Aizawa T
AD  - Department of Orthopaedic Surgery, Tohoku University School of Medicine, Sendai 
      980-8574, Japan.
FAU - Ozawa, Hiroshi
AU  - Ozawa H
AD  - Department of Orthopaedic Surgery, Tohoku Medical and Pharmaceutical University, 
      Sendai 983-8536, Japan.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220402
PL  - Switzerland
TA  - Cells
JT  - Cells
JID - 101600052
SB  - IM
MH  - Autophagy/physiology
MH  - Central Nervous System/metabolism
MH  - *Chaperone-Mediated Autophagy
MH  - Humans
MH  - *Neurodegenerative Diseases/metabolism
MH  - Proteolysis
PMC - PMC8997510
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - Hsc70
OT  - LAMP2A
OT  - Parkinson's disease
OT  - autophagy
OT  - central nervous system
OT  - chaperone-mediated autophagy
OT  - neurodegenerative disease
OT  - spinal cord injury
OT  - traumatic brain injury
COIS- The authors declare no conflict of interest.
EDAT- 2022/04/13 06:00
MHDA- 2022/04/14 06:00
PMCR- 2022/04/02
CRDT- 2022/04/12 01:05
PHST- 2022/02/01 00:00 [received]
PHST- 2022/03/27 00:00 [revised]
PHST- 2022/03/30 00:00 [accepted]
PHST- 2022/04/12 01:05 [entrez]
PHST- 2022/04/13 06:00 [pubmed]
PHST- 2022/04/14 06:00 [medline]
PHST- 2022/04/02 00:00 [pmc-release]
AID - cells11071205 [pii]
AID - cells-11-01205 [pii]
AID - 10.3390/cells11071205 [doi]
PST - epublish
SO  - Cells. 2022 Apr 2;11(7):1205. doi: 10.3390/cells11071205.