Evidence map›Paper›PMID 40145959›Full record

ArticleNeural regeneration research2026

Activin A enhances neurofunctional recovery following traumatic spinal cord injury by inhibiting autophagy.

Liqun Yu, Zhaoyang Yin, Ruiqi Huang, Zhibo Liu, Yuchen Liu, Xinxin Zheng, Simin Song, Zhaojie Wang, Xiaolie He, Yuxin Bai and 5 more

Abstract read
In one paragraph

Article in Neural regeneration research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

15 authors.

Liqun YuKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Zhaoyang YinDepartment of Orthopedics, The First People's Hospital of Lianyungang, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, Jiangsu Province, China.
Ruiqi HuangKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Zhibo LiuKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Yuchen LiuKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Xinxin ZhengKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Simin SongKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Zhaojie WangKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Xiaolie HeKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Yuxin BaiKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Li YangKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Xu XuKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Bairu ChenKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.
Jian YinDepartment of Orthopedics, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Yanjing ZhuKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, School of Medicine, School of Life Science and Technology, Tongji Hospital Affiliated to Tongji University, Tongji University, Shanghai, China.ORCID 0000-0002-2564-1176

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

JOURNAL/nrgr/04.03/01300535-202606000-00063/figure1/v/2026-02-11T151048Z/r/image-tiff In the early stages of traumatic spinal cord injury, extensive accumulation of autophagosomes creates a neurotoxic microenvironment, exacerbating neuronal cell death and worsening tissue damage, ultimately hindering neurofunctional recovery. Activin A is a critical growth factor necessary for the development of the embryonic nervous system and for maintaining neuronal function in the adult cerebral cortex. It can inhibit excessive autophagy in ischemic stroke to reduce neuronal damage. However, the specific mechanism through which Activin A functions in the spinal cord remains poorly understood. In this study, we administered different concentrations of Activin A to neural stem cells from the spinal cord and found that Activin A stimulated the proliferation and neuronal differentiation of neural stem cells. Then, we established an in vitro oxidative stress model by using hydrogen peroxide to stimulate the neural stem cells-induced neurons. We found that Activin A could reduce apoptosis caused by oxidative stress. Subsequently, we treated a mouse model of spinal cord contusion with intrathecal injection of Activin A. Behavioral and electrophysiological results showed that Activin A promoted recovery of motor function and reconstruction of neural circuits in the model mice. Finally, RNA sequencing indicated that Activin A inhibited autophagy by activating the PI3K/AKT/mTOR pathway and upregulating the expression of synaptogenesis-related factor Sema3A in the spinal cord. These results suggest that Activin A may mediate the excessive autophagic response after spinal cord injury, promote the reconstruction of damaged neural circuits, and restore neurological function in the injured spinal cord.

Indexed as

Activin Aautophagycell differentiationmotor function recoveryneural regenerationneural stem cellneuroprotectionphosphoinositide 3-kinase/protein kinase B pathwayspinal cord injurytransforming growth factor-β superfamily

Identifiers

PMID40145959
PMCPMC13211839

What Socratic holds

Textmetadata
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.