Evidence map›Paper›PMID 42760283›Full record

ArticleCommunications biology2026

RhoA in postnatal spinal motoneuron is essential for peripheral myelination.

Ye He, Shuyi Xu, Ying Zou, Mengyao Zhao, Mi Li, Jiale Cai, Xinrui Ma, Anbo Zhang, Xianghai Wang, Jiasong Guo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 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.

Ye He *Department of Histology and Embryology, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, National Demonstration Center for Experimental Education, School of Basic Medical Sciences; Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital; Southern Medical University, Guangzhou, China.
Shuyi Xu *Department of Histology and Embryology, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, National Demonstration Center for Experimental Education, School of Basic Medical Sciences; Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital; Southern Medical University, Guangzhou, China.
Ying ZouDepartment of Histology and Embryology, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, National Demonstration Center for Experimental Education, School of Basic Medical Sciences; Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital; Southern Medical University, Guangzhou, China.
Mengyao ZhaoDepartment of Histology and Embryology, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, National Demonstration Center for Experimental Education, School of Basic Medical Sciences; Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital; Southern Medical University, Guangzhou, China.
Mi LiDepartment of Histology and Embryology, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, National Demonstration Center for Experimental Education, School of Basic Medical Sciences; Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital; Southern Medical University, Guangzhou, China.
Jiale CaiDepartment of Histology and Embryology, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, National Demonstration Center for Experimental Education, School of Basic Medical Sciences; Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital; Southern Medical University, Guangzhou, China.
Xinrui MaDepartment of Histology and Embryology, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, National Demonstration Center for Experimental Education, School of Basic Medical Sciences; Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital; Southern Medical University, Guangzhou, China.
Anbo ZhangDepartment of Histology and Embryology, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, National Demonstration Center for Experimental Education, School of Basic Medical Sciences; Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital; Southern Medical University, Guangzhou, China.
Xianghai WangDepartment of Histology and Embryology, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, National Demonstration Center for Experimental Education, School of Basic Medical Sciences; Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital; Southern Medical University, Guangzhou, China.
Jiasong GuoDepartment of Histology and Embryology, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, National Demonstration Center for Experimental Education, School of Basic Medical Sciences; Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital; Southern Medical University, Guangzhou, China. jiasongguo@smu.edu.cn.ORCID 0000-0002-7885-2903

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peripheral myelination requires precise axon-glia communication, yet the neuronal intrinsic machinery that governs the release of axonal signals remains incompletely understood. Here, we discover that RhoA, a classic cytoskeletal regulator, is highly expressed in postnatal spinal motoneurons and unexpectedly governs this axon-glia communication. RhoA conditional knockout in postnatal motoneurons causes profound peripheral hypomyelination without affecting neuronal survival, dendrites, or axonal caliber. Mechanistically, RhoA deficiency in postnatal spinal motoneurons attenuates ROCK2/p-Erk/SP1/BACE1 signaling and NRG1-Ⅲ secretion, then disrupts Schwann cells differentiation, lipid biosynthesis, and myelin formation. Together, this study reveals a novel, non-cell-autonomous role for RhoA and provides further insights into the complexity of neuronal control over peripheral myelination.

Indexed as

Motor NeuronsMyelin SheathrhoA GTP-Binding Proteinrho GTP-Binding ProteinsSpinal CordAnimalsAxonsCell DifferentiationMiceMice, KnockoutSchwann CellsSignal TransductionrhoA GTP-Binding ProteinRhoA protein, mouserho GTP-Binding Proteins

Identifiers

PMID42760283
PMCPMC13588794

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.