Evidence map›Paper›PMID 40437490›Full record

ArticleJournal of neuroinflammation2025

Impaired membrane lipids in ischemic stroke: a key player in inflammation and thrombosis.

Qian Wang, Dandan Wang, Yan Gao, Jie Jiang, Minghui Li, Shuhui Li, Xiaowen Hu, Jinfeng Wang, Tianqi Wang, Juan Zhang and 5 more

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Qian Wang *Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China.
Dandan Wang *Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China.
Yan GaoBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China.
Jie JiangBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China.
Minghui LiBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China.
Shuhui LiBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China.
Xiaowen HuBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China.
Jinfeng WangBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China.
Tianqi WangBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China.
Juan ZhangBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China.
Lei FengInstrumental Analysis Center, Shanghai Jiao Tong University, Shanghai, 200240, China.
Chao QuanDepartment of Neurology, Shanghai Medical College, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Ping ZhangDepartment of Hyperbaric Oxygen and Neurology, Naval Medical Center of PLA, Naval Medical University, Shanghai, 200052, China.
Lan ZhengDepartment of Neurology, Minhang Hospital, Fudan University, 170 Xinsong Road, Shanghai, 201100, China. zhenglan1323@163.com.
Chunling WanBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 1954 Huashan Road, Shanghai, 200030, China. clwan@sjtu.edu.cn.

Funding

the National Natural Science Foundation of China 82471522the Natural Science Foundation of Shanghai 23ZR1433300the STI2030-Major Projects 2021ZD0200800
6 · The paper itself

Abstract

backgroundMembrane lipids play a crucial role in brain function and cell signalling, and they serve as key biological substrates in inflammatory responses, thrombosis, and energy metabolism. Multiple clinical and molecular evidences suggest that membrane lipids are probably involved in the pathogenesis of ischemic stroke (IS). However, current knowledge about the membrane lipid landscape and its involvement in IS pathophysiology is limited.

methodsWe performed untargeted lipidomic analysis on erythrocyte membranes from 56 IS patients and 55 healthy controls. Integrated with gene expression and weighted gene co-expression network analysis, we identified dysregulated lipid signalling pathways and their contributions to IS pathophysiology.

resultsA total of 1392 erythrocyte membrane lipids were detected and quantified. Our results revealed significant impairment of membrane lipid homeostasis in IS patients, characterized by a marked reduction in glycerophospholipids (GPLs) and lysophospholipids (LPLs). Further analysis indicated that the impaired lipids were primarily concentrated in three disturbed signalling pathways, including the phospholipase A2-mediated GPL-LPL pathway, the phospholipase C-mediated inositol 1,4,5-trisphosphate/diglyceride pathway, and the sphingosine-1-phosphate (S1P)-S1P receptors pathway. Gene expression results indicated that these pathways were inhibited during the subacute phase of IS. Furthermore, these lipid signalling pathways form a highly interconnected network that collaboratively contributes to inflammation and thrombosis in IS, thereby influencing the progression and prognosis of the disease.

conclusionOur findings reveal impaired erythrocyte membrane lipid homeostasis in IS, which implicates inflammatory processes and thrombosis in IS. This research offers new insights into the role of membrane lipids in IS pathogenesis, potentially informing future monitoring and therapeutic strategies.

Indexed as

Erythrocyte MembraneInflammationIschemic StrokeMembrane LipidsThrombosisAgedFemaleHumansLipidomicsMaleMiddle AgedSignal TransductionMembrane LipidsInflammationIschemic strokeLipidomeLipid signalling pathwayMembrane lipidsThrombosis

Identifiers

PMID40437490
PMCPMC12117946

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.