Evidence map›Paper›PMID 40474194›Full record

ArticleJournal of neuroinflammation2025

Circulating T cell atlas in Moyamoya disease: insights into immunopathogenesis of cerebrovascular disorders.

Chenglong Liu, Junsheng Li, Siqi Mou, Yuheng Pang, Liujia Chan, Qiheng He, Wei Liu, Zhikang Zhao, Bojian Zhang, Zhiyao Zheng and 8 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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Observational
  3. Article
  4. Article
  5. Article
  6. Review
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

18 authors.

Chenglong Liu *Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Junsheng Li *Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Siqi Mou *Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Yuheng PangBeijing YouAn Hospital, Beijing Institute of Hepatology, Capital Medical University, Beijing, 100069, China.
Liujia ChanDepartment of Medicinal Chemistry, College of Pharmaceutical Sciences, Capital Medical University, Beijing, 100069, P. R. China.
Qiheng HeDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Wei LiuDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Zhikang ZhaoDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Bojian ZhangDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Zhiyao ZhengDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Wei SunDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Xiangjun ShiChina National Clinical Research Center for Neurological Diseases, Beijing, 100070, China.
Qian ZhangDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Rong WangDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Yan ZhangDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Wenjing WangBeijing YouAn Hospital, Beijing Institute of Hepatology, Capital Medical University, Beijing, 100069, China. wangwenjing85321@ccmu.edu.cn.
Dong ZhangDepartment of Neurosurgery, Beijing Hospital, National Center of Gerontology, Beijing, 100730, China. zhangdong0660@aliyun.com.
Peicong GeDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China. gepeicong@163.com.

Funding

National Natural Science Foundation of China 82301451
6 · The paper itself

Abstract

backgroundMoyamoya disease (MMD) is a chronic cerebrovascular disorder characterized by progressive stenosis or occlusion of the intracranial arteries, accompanied by the formation of fragile collateral vessels, ultimately leading to ischemic or hemorrhagic strokes. Immune dysregulation, particularly involving T cell abnormalities and mitochondrial dysfunction, plays a critical role in the pathogenesis of MMD; however, their precise relationship remains unclear.

methodsPeripheral blood mononuclear cells (PBMCs) from patients with MMD and healthy controls were analyzed using mass cytometry (CyTOF) and transcriptomic profiling. Additionally, clinical characteristics and neuroimaging data were collected to perform integrated correlation analyses with immune profiling data.

resultsPatients with MMD exhibited aberrant T cell activation and altered subset distribution, accompanied by mitochondrial dysfunction and impaired oxidative phosphorylation capacity. Increased oxidative stress and endoplasmic reticulum stress were observed in T cells, along with disease-specific downregulation of immune checkpoint molecules, including PD-1 and ICOS.

conclusionsThis study highlights the critical involvement of immune activation and mitochondrial dysfunction in the pathophysiology of MMD, providing novel insights into disease mechanisms and identifying immunometabolic pathways as potential targets for therapeutic intervention.

Indexed as

Cerebrovascular DisordersMoyamoya DiseaseT-LymphocytesAdultFemaleHumansLeukocytes, MononuclearMaleMiddle AgedMitochondriaOxidative StressYoung AdultImmunometabolismMass cytometryMitochondrial dysfunctionMoyamoya diseaseT cells

Identifiers

PMID40474194
PMCPMC12142972

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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 OpenQuestion graph.