兰州大学机构库
TREM2, microglial and ischemic stroke
Wang, Hongxia1; Li, Xiaoling1; Wang, Qi1; Ma, Jialiang1; Gao, Xiaohong2; Wang, Manxia1
2023-08-15
Online publication date2023-06
Source PublicationJOURNAL OF NEUROIMMUNOLOGY   Impact Factor & Quartile
ISSN0165-5728 ; 1872-8421
Volume381
page numbers13
AbstractIschemic stroke (IS) is a leading cause of morbidity and mortality worldwide. Immunity and inflammation are key factors in the pathophysiology of IS. The inflammatory response is involved in all stages of stroke, and microglia are the predominant cells involved in the post-stroke inflammatory response. Resident microglia are the main immune cells of the brain and the first line of defense of the nervous system. After IS, activated microglia can be both advantageous and detrimental to surrounding tissue; they can be divided into the harmful M1 types or the neuro-protective M2 type. Currently, with the latest progress of transcriptomics analysis, different and more complex phenotypes of microglia activation have been described, such as disease-related microglia (DAM) associated with Alzheimer's disease (AD), white matter associated microglia (WAMs) in aging, and stroke-related microglia (SAM) etc. The triggering receptor expressed on myeloid cell 2 (TREM2) is an immune-related receptor on the surface of microglia. Its expression increases after IS, which is related to microglial inflammation and phagocytosis, however, its relationship with the microglia phenotype is not clear. This paper reviews the following: 1) the phenotypic changes of microglia in various pathological stages after IS and its relationship with inflammatory factors; 2) the relationship between the expression of the TREM2 receptor and inflammatory factors; 3) the relationship between phenotypic changes of microglia and its surface receptor TREM2; 4) the TREM2-related signalling pathway of microglia after IS and treatment for TREM2 receptor; and finally 5) To clarify the relationship among TREM2, inflammation, and microglia phenotype after IS, as well as the mechanism among them and the some possible treatment of IS targeting TREM2. Moreover, the relationship between the new phenotype of microglia such as SAM and TREM2 has also been systematically summarized, but there are no relevant research reports on the relationship between TREM2 and SAM after IS.
KeywordTREM2 Ischemic stroke Immunity and inflammation Microglia phenotype
PublisherELSEVIER
DOI10.1016/j.jneuroim.2023.578108
Indexed BySCIE
Language英语
WOS Research AreaImmunology ; Neurosciences & Neurology
WOS SubjectImmunology ; Neurosciences
WOS IDWOS:001021542200001
Original Document TypeReview
PMID 3730217
Citation statistics
Cited Times:4[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttps://ir.lzu.edu.cn/handle/262010/569666
Collection兰州大学
第二临床医学院
Corresponding AuthorWang, Manxia
Affiliation
1.Lanzhou Univ, Dept Neurol, Hosp 2, Cuiyingmen 82, Lanzhou 730030, Gansu, Peoples R China;
2.Wuwei peoples Hosp, Dept Neurol, North Side Xuanwu St, Wuwei 733000, Gansu, Peoples R China
First Author AffilicationSecond Clinical School
Corresponding Author AffilicationSecond Clinical School
Recommended Citation
GB/T 7714
Wang, Hongxia,Li, Xiaoling,Wang, Qi,et al. TREM2, microglial and ischemic stroke[J]. JOURNAL OF NEUROIMMUNOLOGY,2023,381.
APA Wang, Hongxia,Li, Xiaoling,Wang, Qi,Ma, Jialiang,Gao, Xiaohong,&Wang, Manxia.(2023).TREM2, microglial and ischemic stroke.JOURNAL OF NEUROIMMUNOLOGY,381.
MLA Wang, Hongxia,et al."TREM2, microglial and ischemic stroke".JOURNAL OF NEUROIMMUNOLOGY 381(2023).
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