题名 | Functions and mechanisms of cytosolic phospholipase A2 in central nervous system trauma. |
作者 | |
发表日期 | 2023-02 |
发表期刊 | Neural regeneration research 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Journal Article ; Review |
关键词 | autophagy {"sub":"2"} drugs lysosome membrane permeability mitogen-activated protein kinase neuroinflammation spinal cord injury traumatic brain injury cytosolic phospholipase A_2 |
其他关键词 | SPINAL-CORD-INJURY ; ACTIVATED PROTEIN-KINASE ; ARACHIDONIC-ACID RELEASE ; ISCHEMIC BRAIN-DAMAGE ; INFLAMMATORY RESPONSE ; REDUCES INFLAMMATION ; SIGNALING PATHWAY ; A(2) SUPERFAMILY ; IN-VITRO ; AUTOPHAGY |
摘要 | {AbstractText=Central nervous system (CNS) trauma, including traumatic brain injury and spinal cord injury, has a high rate of disability and mortality, and effective treatment is currently lacking. Previous studies have revealed that neural inflammation plays a vital role in CNS trauma. As the initial enzyme in neuroinflammation, cytosolic phospholipase A2 (cPLA2) can hydrolyze membranous phosphatides at the sn-2 position in a preferential way to release lysophospholipids and ω3-polyunsaturated fatty acid dominated by arachidonic acid, thereby inducing secondary injuries. Although there is substantial fresh knowledge pertaining to cPLA2, in-depth comprehension of how cPLA2 participates in CNS trauma and the potential methods to ameliorate the clinical results after CNS trauma are still insufficient. The present review summarizes the latest understanding of how cPLA2 participates in CNS trauma, highlighting novel findings pertaining to how cPLA2 activation initiates the potential mechanisms specifically, neuroinflammation, lysosome membrane functions, and autophagy activity, that damage the CNS after trauma. Moreover, we focused on testing a variety of drugs capable of inhibiting cPLA2 or the upstream pathway, and we explored how those agents might be utilized as treatments to improve the results following CNS trauma. This review aimed to effectively understand the mechanism of cPLA2 activation and its role in the pathophysiological processes of CNS trauma and provide clarification and a new referential framework for future research.} |
资助项目 | supported by the National Natural Science Foundation of China,No.82072192 (to KLZ);; Public Welfare Technology Research Project of Zhejiang Province,No.LGF20H150003 (to KLZ);; the Natural Science Foundation of Zhejiang Province,Nos.LY17H060009 and Y21H060050 (both to WFN);; Wenzhou Science and Technology Bureau Foundation,No.Y20210438 (to KLZ) |
出版者 | WOLTERS KLUWER MEDKNOW PUBLICATIONS |
ISSN | 1673-5374 |
EISSN | 1876-7958 |
卷号 | 18期号:2页码:258-266 |
DOI | 10.4103/1673-5374.346460 |
页数 | 9 |
WOS类目 | Cell Biology ; Neurosciences |
WOS研究方向 | Cell Biology ; Neurosciences & Neurology |
WOS记录号 | WOS:000834672700004 |
收录类别 | PUBMED ; SCOPUS ; SCIE ; CNKI |
URL | 查看原文 |
PubMed ID | 35900400 |
SCOPUSEID | 2-s2.0-85135484629 |
ESI高被引论文 | 2023-07 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/155388 |
专题 | 第二临床医学院、附属第二医院、育英儿童医院 |
通讯作者 | Ni, Wen-Fei; Zhou, Kai-Liang |
作者单位 | 1.Wenzhou Med Univ, Affiliated Hosp 2, Dept Orthoped, Wenzhou, Zhejiang, Peoples R China; 2.Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou, Zhejiang, Peoples R China; 3.Zhejiang Prov Key Lab Orthoped, Wenzhou, Zhejiang, Peoples R China; 4.Wenzhou Med Univ, Clin Med Coll 2, Wenzhou, Zhejiang, Peoples R China |
第一作者单位 | 第二临床医学院,附属第二医院、育英儿童医院; 附属第二医院 |
第一作者的第一单位 | 第二临床医学院,附属第二医院、育英儿童医院 |
推荐引用方式 GB/T 7714 | Zhang, Hao-Jie,Chen, Yi-Tuo,Hu, Xin-Li,et al. Functions and mechanisms of cytosolic phospholipase A2 in central nervous system trauma.[J]. Neural regeneration research,2023,18(2):258-266. |
APA | Zhang, Hao-Jie., Chen, Yi-Tuo., Hu, Xin-Li., Cai, Wan-Ta., Wang, Xiang-Yang., ... & Zhou, Kai-Liang. (2023). Functions and mechanisms of cytosolic phospholipase A2 in central nervous system trauma.. Neural regeneration research, 18(2), 258-266. |
MLA | Zhang, Hao-Jie,et al."Functions and mechanisms of cytosolic phospholipase A2 in central nervous system trauma.".Neural regeneration research 18.2(2023):258-266. |
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