Evidence map›Paper›PMID 42559269›Full record

ArticleTheranostics2026

Targeting microglial MyD88 reprograms injury-activated microglia and promotes spinal cord repair via TGF-β signaling and biomimetic nanodelivery.

Jintao Liu, Beibei Yu, Wanjun Cao, Jilu Liu, Yundi Gao, Honghui Mao, Xiaochuan Gao, Lingli Guo, Shengyou Li, Qiao Huang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Theranostics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Jintao LiuDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Beibei YuDepartment of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Wanjun CaoDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Jilu LiuDepartment of Orthopedics, Naval Hospital of Eastern Theater, Zhoushan 316000, China.
Yundi GaoSeventh Squad, Second Regiment, Basic Medical College, Fourth Military Medical University, Xi'an 710032, China.
Honghui MaoDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Xiaochuan GaoDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Lingli GuoDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Shengyou LiDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Qiao HuangDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Mingze QinDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Fang KuangDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China.
Jinghui HuangDepartment of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Following spinal cord injury (SCI), activated microglia sustain neuroinflammation and drive secondary tissue damage, and this limits functional recovery. Myeloid differentiation primary response 88 (MyD88) is a central adaptor of innate immune signaling, but whether and how microglial MyD88 regulates state transition after SCI remains unclear. This study aims to explore the impact of microglial MyD88 signaling on microglial state trajectories and tissue repair after SCI and to develop a microglia-targeted delivery strategy for therapeutic modulation. Methods: A forceps-mediated SCI mouse model was established, and bulk and single-cell RNA sequencing were used to profile the temporal activation of microglial MyD88 signaling in the spinal cord. Pharmacological MyD88 inhibition (ST2825) and inducible microglia-specific MyD88 conditional knockout mice ( Results: Transcriptomic analyses revealed rapid and sustained activation of MyD88 signaling preferentially in microglia after SCI. ST2825 suppressed pro-inflammatory outputs Conclusion: Our data establish MyD88 as a critical regulator of microglial reprogramming after SCI and highlight its potential as a therapeutic target for spinal cord repair.

Indexed as

MicrogliaMyeloid Differentiation Factor 88Spinal Cord InjuriesSpinal Cord RegenerationTransforming Growth Factor betaAnimalsBiomimeticsDisease Models, AnimalFemaleHeterocyclic Compounds, 2-RingMiceMice, Inbred C57BLMice, KnockoutNanoparticlesRecovery of FunctionSignal TransductionHeterocyclic Compounds, 2-RingMyd88 protein, mouseMyeloid Differentiation Factor 88Spiro CompoundsST2825Transforming Growth Factor betabiomimetic nanoparticlemicroglial state transitionMyD88spinal cord injuryTGF-β

Identifiers

PMID42559269
PMCPMC13440466

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Registered trials

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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.