Evidence map›Paper›PMID 41697574›Full record

ReviewNeuroscience bulletin2026

Reactive OPCs in CNS Injury: From Functional Diversity to Therapeutic Translation.

Shengnan Wang, Hong Liu, Jiali Li, Yimin Yuan, Ziwei Dai, Zhida Lan, Chao Huang, Xiaojie Wei, Cheng He, Zhida Su and 1 more

Abstract readReview
In one paragraph

Review in Neuroscience bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Shengnan Wang *Department of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China.
Hong Liu *Department of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China.
Jiali LiDepartment of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China.
Yimin YuanDepartment of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China.
Ziwei DaiDepartment of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China.
Zhida LanDepartment of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China.
Chao HuangDepartment of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China.
Xiaojie WeiDepartment of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China.
Cheng HeDepartment of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China.
Zhida SuDepartment of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China. suzhida@smmu.edu.cn.ORCID http://orcid.org/0000-0003-3512-476X
Shangyao QinDepartment of Neurobiology, College of Basic Medicine, Key Laboratory of Molecular Neurobiology of the Ministry of Education, Naval Medical University, Shanghai, 200433, China. shangyao_qin@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Central nervous system (CNS) injuries trigger a complex glial response, in which oligodendrocyte precursor cells (OPCs) play a far more dynamic role than previously recognized. Moving beyond their canonical function as a remyelination reservoir, reactive OPCs emerge as plastic signaling hubs whose fate and function are dictated by injury-specific cues. This review synthesizes recent evidence to propose a novel conceptual framework: the "reactive OPC state code." We argue that deciphering this code-the molecular signatures that define pro-regenerative, immunomodulatory, or maladaptive OPC states-is the key to understanding functional heterogeneity in CNS injury. We critically analyze how distinct pathological contexts (trauma, ischemia, neuroinflammation) rewrite this code, leading to diverse outcomes. Finally, we pivot from a generic discussion of OPC-directed therapies to advocate for "state-specific targeting" as the next frontier in translational medicine, offering a roadmap for developing precision interventions that steer reactive OPCs towards repair. This perspective aims to redefine OPC reactivity from a passive response to a central, druggable axis in CNS pathology and repair.

Indexed as

Central Nervous SystemCentral Nervous System DiseasesOligodendrocyte Precursor CellsAnimalsHumansNerve RegenerationOligodendrogliaRemyelinationCellular plasticityCellular reactivityCentral nervous system injuryOligodendrocyte precursor cellsRemyelination

Identifiers

PMID41697574
PMCPMC13388883

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.