Evidence mapPaperPMID 41606721Full record

ReviewThe journal of headache and pain2026

Targeting glial-orchestrated neuroinflammation in migraine pathophysiology.

Weiwei Lu, Yuan Zhang, Chen Shi, Yu Tao, Shaoxin Li, Yufang Sun, Fuhai Ji, Gang Chen, Terrance P Snutch, Jin Tao

Abstract readReview
In one paragraph

Review in The journal of headache and pain, 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

10 authors.

Weiwei Lu *The First Affiliated Hospital of Soochow University, School of Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, 215123, P.R., China. wwlu@suda.edu.cn.
Yuan Zhang *Clinical Research Center of Neurological Disease, Department of Geriatrics, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, P.R., China. yuanzhang@suda.edu.cn.
Chen Shi *The First Affiliated Hospital of Soochow University, School of Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, 215123, P.R., China.
Yu TaoThe First Affiliated Hospital of Soochow University, School of Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, 215123, P.R., China.
Shaoxin LiThe First Affiliated Hospital of Soochow University, School of Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, 215123, P.R., China.
Yufang SunThe First Affiliated Hospital of Soochow University, School of Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, 215123, P.R., China.
Fuhai JiDepartment of Anesthesiology, The First Affiliated Hospital of Soochow University, Suzhou, 215006, P.R., China.
Gang ChenDepartment of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, P.R., China.
Terrance P SnutchMichael Smith Laboratories, University of British Columbia, Vancouver, British Columbia, V6T 1Z4, Canada.
Jin TaoThe First Affiliated Hospital of Soochow University, School of Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, 215123, P.R., China. taoj@suda.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMigraine is a chronic neurological disorder characterized by severe headache, nausea, and sensitivity to light and sound, affecting approximately 1 billion people globally. Despite advances in understanding migraine pathophysiology, particularly with the emergence of CGRP-targeted therapies, the mechanisms underlying neuroinflammation and glial contributions remain poorly understood. Current treatments are effective for a subset of patients, yet they don’t tackle the fundamental neurogenic and neuroinflammatory processes that fuel chronic migraine, especially the pathophysiological aspects contributed by glial cells. PRINCIPAL

findingsThis review integrates recent preclinical and clinical evidence to elucidate how diverse glial cells, including central glia (astrocytes, microglia and oligodendrocytes) and peripheral glia (Schwann cells, satellite glial cells), coordinate the neuroinflammation associated with migraine. Evidence shows that astrocytes and microglia are essential to both cortical spreading depolarization (CSD) and mediating the inflammatory cascades that maintain chronic pain. Oligodendrocytes, though less studied, are predicted to affect neuronal excitability and energy metabolism, while Schwann cells and satellite glial cells mediate peripheral nociceptive signaling through their interactions with neural and immune elements. New therapeutic strategies have been put forward. These include targeting glial-specific signaling pathways and employing advanced drug delivery systems such as viral vectors and nanoparticles to improve treatment effectiveness.

conclusionGlial cells are pivotal regulators of migraine-associated neuroinflammation. This review underscores their critical role in migraine pathophysiology and highlights glial-targeted therapies as a promising direction for future research and treatment development.

Indexed as

Migraine DisordersNeurogliaNeuroinflammatory DiseasesAnimalsHumansCellular mechanismsGlial cellsMigraineNeuro-immune axisTrigeminovascular system

Identifiers

PMID41606721
PMCPMC12924293

What Socratic holds

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LicenceCC BY-NC-ND
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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.