PMID- 38395207
OWN - NLM
STAT- MEDLINE
DCOM- 20240327
LR  - 20240327
IS  - 1096-1186 (Electronic)
IS  - 1043-6618 (Linking)
VI  - 202
DP  - 2024 Apr
TI  - Unveiling the role of iPLA(2)beta in neurodegeneration: From molecular mechanisms to 
      advanced therapies.
PG  - 107114
LID - S1043-6618(24)00058-6 [pii]
LID - 10.1016/j.phrs.2024.107114 [doi]
AB  - Calcium-independent phospholipase A(2)beta (iPLA(2)beta), a member of the phospholipase 
      A2 (PLA2s) superfamily, is encoded by the PLA2G6 gene. Mutations in the PLA2G6 
      gene have been identified as the primary cause of infantile neuroaxonal dystrophy 
      (INAD) and, less commonly, as a contributor to Parkinson's disease (PD). Recent 
      studies have revealed that iPLA(2)beta deficiency leads to neuroinflammation, iron 
      accumulation, mitochondrial dysfunction, lipid dysregulation, and other 
      pathological changes, forming a complex pathogenic network. These discoveries 
      shed light on potential mechanisms underlying PLA2G6-associated neurodegeneration 
      (PLAN) and offer valuable insights for therapeutic development. This review 
      provides a comprehensive analysis of the fundamental characteristics of iPLA(2)beta, 
      its association with neurodegeneration, the pathogenic mechanisms involved in 
      PLAN, and potential targets for therapeutic intervention. It offers an overview 
      of the latest advancements in this field, aiming to contribute to ongoing 
      research endeavors and facilitate the development of effective therapies for 
      PLAN.
CI  - Copyright (c) 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.
FAU - Liu, Jiabin
AU  - Liu J
AD  - Department of Neurology, Xiangya Hospital, Central South University, Changsha, 
      Hunan, China.
FAU - Tan, Jieqiong
AU  - Tan J
AD  - Centre for Medical Genetics and Hunan Key Laboratory of Medical Genetics, School 
      of Life Sciences, Central South University, Changsha, Hunan 410008, China.
FAU - Tang, Beisha
AU  - Tang B
AD  - Department of Neurology, Xiangya Hospital, Central South University, Changsha, 
      Hunan, China; Department of Geriatrics, Xiangya Hospital, Central South 
      University, Changsha, Hunan, China; National Clinical Research Center for 
      Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, 
      China.
FAU - Guo, Jifeng
AU  - Guo J
AD  - Department of Neurology, Xiangya Hospital, Central South University, Changsha, 
      Hunan, China; Centre for Medical Genetics and Hunan Key Laboratory of Medical 
      Genetics, School of Life Sciences, Central South University, Changsha, Hunan 
      410008, China; National Clinical Research Center for Geriatric Disorders, Xiangya 
      Hospital, Central South University, Changsha, Hunan, China. Electronic address: 
      guojifeng@csu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20240222
PL  - Netherlands
TA  - Pharmacol Res
JT  - Pharmacological research
JID - 8907422
SB  - IM
MH  - *Mutation
OTO - NOTNLM
OT  - IPLA(2)beta
OT  - Lipid
OT  - Mitochondria
OT  - Neurodegeneration
OT  - PLA2G6
COIS- Declaration of Competing Interest None.
EDAT- 2024/02/24 11:42
MHDA- 2024/03/27 06:43
CRDT- 2024/02/23 19:15
PHST- 2023/10/18 00:00 [received]
PHST- 2024/02/08 00:00 [revised]
PHST- 2024/02/20 00:00 [accepted]
PHST- 2024/03/27 06:43 [medline]
PHST- 2024/02/24 11:42 [pubmed]
PHST- 2024/02/23 19:15 [entrez]
AID - S1043-6618(24)00058-6 [pii]
AID - 10.1016/j.phrs.2024.107114 [doi]
PST - ppublish
SO  - Pharmacol Res. 2024 Apr;202:107114. doi: 10.1016/j.phrs.2024.107114. Epub 2024 
      Feb 22.