Evidence map›Paper›PMID 41995115›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Prmt6 Deficiency or Inhibition Restores Microglial Homeostasis and Promotes Scar-Limited Repair in Adult Spinal Cord Injury.

Weilin Peng, Zhengqiang Wu, Yu Xiong, Zhongya Gao, Yishan Liu, Ziyi Wang, Haibin Wang, Chaofeng Han, Wenxiang Chu, Xuhua Lu

Abstract read
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In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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

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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

10 authors.

Weilin PengDepartment of Orthopaedics, Changzheng Hospital, Naval Medical University, Shanghai, China.
Zhengqiang WuDepartment of Orthopaedics, Changzheng Hospital, Naval Medical University, Shanghai, China.
Yu XiongDepartment of Orthopaedics, Changzheng Hospital, Naval Medical University, Shanghai, China.
Zhongya GaoDepartment of Orthopaedics, Changzheng Hospital, Naval Medical University, Shanghai, China.
Yishan LiuDepartment of Orthopaedics, Changzheng Hospital, Naval Medical University, Shanghai, China.ORCID https://orcid.org/0009-0007-0156-2354
Ziyi WangDepartment of Histology and Embryology, National Key Laboratory of Immunity and Inflammation, Naval Medical University, Shanghai, China.
Haibin WangDepartment of Orthopaedics, Changzheng Hospital, Naval Medical University, Shanghai, China.
Chaofeng HanDepartment of Histology and Embryology, National Key Laboratory of Immunity and Inflammation, Naval Medical University, Shanghai, China.
Wenxiang ChuDepartment of Orthopaedics, Changzheng Hospital, Naval Medical University, Shanghai, China.
Xuhua LuDepartment of Orthopaedics, Changzheng Hospital, Naval Medical University, Shanghai, China.ORCID https://orcid.org/0000-0002-8400-8960

Funding

Matching Research Funds for High-Level Talent Recruitment of Changzheng Hospital 2024GCCRC-303National Key R&D Program of China 2024YFA0918400National Natural Science Foundation of China 31970853National Natural Science Foundation of China 32170878National Natural Science Foundation of China 81572201National Natural Science Foundation of China 81802185Research Projects of Shanghai Changzheng Hospital 0901Research Projects of Shanghai Changzheng Hospital 2020YCXYJ-ZD06Shanghai Leading Talent Program of Eastern Talent Plan SHSDFYCBJ-LXH
6 · The paper itself

Abstract

Neonatal mice achieve scar-free healing after spinal cord injury (SCI) by restoring microglial homeostasis, unlike adults, where persistent microglial dyshomeostasis drives scar expansion through mechanisms that remain elusive. Using RNA sequencing, we identified protein arginine methyltransferase 6 (PRMT6) as a key regulator of this disparity, upregulated in activated microglia at adult SCI lesions but maintained at low levels in neonatal microglia after injury. In adult mice, Prmt6 deficiency restored microglial homeostasis, evidenced by increased P2Y12/TMEM119 and reduced CD68, while reducing scar formation and enhancing axonal regrowth and motor recovery. Microglia-specific Prmt6 knockdown or PRMT6 inhibitor administration recapitulated these effects. Mechanistically, PRMT6 deposits H3R2me2a at the Ppargc1a promoter to repress peroxisome proliferator-activated receptor-γ coactivator-1α（PGC-1α）, thereby inhibiting fatty acid oxidation (FAO) and disrupting microglial homeostasis. Loss of Prmt6 alleviates this epigenetic repression, restoring FAO and microglial homeostasis. These findings establish PRMT6 as a novel epigenetic regulator linking microglial dyshomeostasis and metabolic dysfunction to maladaptive scar formation in adult SCI, highlighting PRMT6 inhibition as a promising therapeutic strategy to reprogram microglial metabolism and promote neural repair.

Indexed as

CicatrixHomeostasisMicrogliaProtein-Arginine N-MethyltransferasesSpinal Cord InjuriesAnimalsDisease Models, AnimalMiceProtein-Arginine N-Methyltransferasesfatty acid oxidationhomeostasismicrogliaPGC‐1αspinal cord injury

Identifiers

PMID41995115
PMCPMC13335747

What Socratic holds

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LicenceCC BY
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.