Evidence map›Paper›PMID 41390720›Full record

ArticleMolecular neurodegeneration2025

Targeted deletion of EMMPRIN in microglia/macrophages mitigates neuronal death in intracerebral hemorrhage.

Zhe Li, Xiangyu Zhang, Maryam Mobarakabadi, Yang Liu, Ruixue Wei, Claudia Silva, Frank Visser, Antoine Dufour, Daniel Young, Deepak Kaushik and 2 more

Abstract read
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In one paragraph

Article in Molecular neurodegeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Zhe LiDepartment of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Xiangyu ZhangDepartment of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Maryam MobarakabadiHotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada.
Yang LiuDepartment of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Ruixue WeiDepartment of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Claudia SilvaHotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada.
Frank VisserHotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada.
Antoine DufourHotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada.
Daniel YoungDepartments of Biochemistry and Molecular Biology, and Physiology and Pharmacology, and McCaig Institute for Bone and Joint Health, University of Calgary, Calgary, Canada.
Deepak KaushikDivision of Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.
V Wee YongHotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. vyong@ucalgary.ca.
Mengzhou XueDepartment of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. xuemengzhou@zzu.edu.cn.

Funding

CIHR 1049959National Natural Science Foundation of China Youth Program 82401559 and 82402350the National Natural Science Foundation of China 82071331, 81870942, and 81520108011
6 · The paper itself

Abstract

backgroundIntracerebral hemorrhage (ICH) is a devastating subtype of stroke with high mortality and limited therapeutic options. Microglia and macrophages are rapidly recruited to the lesion site and contribute substantially to secondary brain injury. However, the key molecular mediators that drive their neurotoxic effects remain incompletely understood.

methodsWe investigated the role of extracellular matrix metalloproteinase inducer (EMMPRIN, also known as CD147) in promoting microglia/macrophage-mediated neurotoxicity after ICH. EMMPRIN was selectively deleted in myeloid cells using both AAV-mediated knockdown and CX3CR1Cre:EMMPRINfl/fl mice. Neuronal survival and functional outcomes were assessed using histological, molecular, and behavioral analyses.

resultsTargeted deletion of EMMPRIN in microglia/macrophages significantly reduced neuronal death and improved neurological recovery following ICH. Mechanistically, EMMPRIN-mediated neurotoxicity was associated with elevated expression of matrix metalloproteinases and enhanced activation of the p38 mitogen-activated protein kinase (MAPK) pathway, and with downstream engagement of myocyte enhancer factor 2 C (MEF2C) and B-cell lymphoma 2 (Bcl2). Notably, EMMPRIN deletion also enhanced neurogenesis and oligodendrogenesis in the perihematomal region, suggesting a potential role in promoting endogenous brain repair.

conclusionsThese findings establish EMMPRIN elevation in myeloid cells as a prominent regulator of ICH pathophysiology and a promising therapeutic target to limit secondary injury and promote brain repair.

Indexed as

BasiginCerebral HemorrhageMacrophagesMicrogliaNeuronsAnimalsCell DeathDisease Models, AnimalMaleMiceBasiginBsg protein, mouseEMMPRINIntracerebral hemorrhageMatrix metalloproteinasesMicroglia/macrophagesNeuroprotectionRegeneration

Identifiers

PMID41390720
PMCPMC12817446

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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.