Evidence map›Paper›PMID 42212054›Full record

ReviewJournal of orthopaedic translation2026

Targeting the glial-fibrotic scar microenvironment after spinal cord injury: From integrated protection to systematic regulation of regenerative balance.

Zhaoliang Hou, Shenghui Shang, Haijian Sun, Yixiao He, Sen Guo, Mingjie Sun, Xiumei Tang, Zhijian Wei, Wenzhao Wang, Bin Ning

Abstract readReview
In one paragraph

Review in Journal of orthopaedic translation, 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. Article
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.

Zhaoliang HouDepartment of Orthopaedics, Jinan Central Hospital, Shandong University, Jinan, Shandong, 250013, China.
Shenghui ShangDepartment of Orthopaedics, Qilu Hospital, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China.
Haijian SunThe Second Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250013, China.
Yixiao HeDepartment of Orthopaedics, Jinan Central Hospital, Shandong University, Jinan, Shandong, 250013, China.
Sen GuoDepartment of Pathology, Department of Radiology, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Mingjie SunDepartment of Orthopaedics, Jinan Central Hospital, Shandong University, Jinan, Shandong, 250013, China.
Xiumei TangHealth Management Center, General Practice Medical Center, Institute of Hospital Management, West China Hospital, Sichuan University, Chengdu, 610041, China.
Zhijian WeiDepartment of Orthopaedics, Qilu Hospital, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China.
Wenzhao WangDepartment of Orthopaedics, Jinan Central Hospital, Shandong University, Jinan, Shandong, 250013, China.
Bin NingDepartment of Orthopaedics, Jinan Central Hospital, Shandong University, Jinan, Shandong, 250013, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spinal cord injury (SCI) represents a severe neurological disorder characterized by complex pathophysiological cascades, frequently resulting in irreversible sensorimotor deficits. A hallmark of this condition is the dual-phase response of glial and fibrotic scars: initially, reactive astrocytes and fibroblast-like cells form protective barriers that limit inflammatory spread and stabilize tissue integrity, yet chronically, these scars transition into inhibitory structures through excessive deposition of chondroitin sulfate proteoglycans (CSPGs) and collagen-rich extracellular matrix (ECM), obstructing axonal regeneration. Critically, these scars operate within an integrated SCI scar microenvironment, where multiple cellular, molecular, and matrix components dynamically and coordinately modulate their reparative-to-pathological shift. This review systematically examines the spatiotemporal organization, cellular heterogeneity, and molecular drivers underlying scar duality. We evaluate bidirectional interactions between glial and fibrotic components and non-scar elements. Notably, the scar microenvironment serves as a pivotal regulatory hub that dictates the switch between the protective and inhibitory phenotypes of scars post-SCI. This work underscores the scar microenvironment's centrality in SCI pathology and advances the conceptual framework for developing precision therapies to overcome neuroregenerative failure. The Translational Potential of this Article: This review's spinal cord injury scar microenvironment theory delivers a transformative translational framework. It captures spatiotemporal crosstalk of cellular, molecular, and matrix components across injury phases, replacing fragmented single-target interventions. Representative translational strategies include artificial spinal cord ECM hydrogels, Induced Pluripotent Stem Cells (iPSCs) derived spinal cord organoid transplantation, exosome-mediated epigenetic regulation, among others, which are all aligned with pathological progression. Supported by international Phase I/II clinical trials targeting scar microenvironment components, this theory integrates basic research with clinical needs. It enables precision SCI therapy through coordinated intervention logic, accelerating the translation from symptomatic management to curative neural repair.

Indexed as

Chondroitin sulfate proteoglycansFibrotic scarGlial scarScar microenvironmentSpinal cord injuryTargeted therapy

Identifiers

PMID42212054
PMCPMC13213693

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.