Evidence map›Paper›PMID 40000609›Full record

ArticleCell death & disease2025

Bone marrow mesenchymal stem cells alleviate neurological dysfunction by reducing autophagy damage via downregulation of SYNPO2 in neonatal hypoxic-ischemic encephalopathy rats.

Lu- Lu Xue, Jie Cheng, Ruo-Lan Du, Bo-Yan Luo, Li Chen, Qiu-Xia Xiao, Hong-Su Zhou, Hong-Qing She, Shi-Feng Wang, Ting-Bao Chen and 4 more

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Alterations ofCurrent Alzheimer research · 2025
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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

14 authors.

Lu- Lu Xue *Department of Anesthesiology, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China.
Jie Cheng *Center for Reproductive Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Ruo-Lan DuDepartment of Anesthesiology, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China.
Bo-Yan LuoSchool of Pharmacy, Zunyi Medical University, Zunyi, Guizhou, China.
Li ChenDepartment of Neurosurgery, Institute of Neurological Disease, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Qiu-Xia XiaoDepartment of Anesthesiology, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China.
Hong-Su ZhouDepartment of Anesthesiology, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China.
Hong-Qing SheDepartment of Anesthesiology, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China.
Shi-Feng WangDepartment of Anesthesiology, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China.
Ting-Bao ChenInstitute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.
Chang-Yan HuInstitute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.
Yu-Qi HeDepartment of Anesthesiology, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China. hyqjeff@foxmail.com.
Ting-Hua WangDepartment of Anesthesiology, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China. wangtinghua@vip.163.com.
Liu-Lin XiongDepartment of Anesthesiology, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China. 499465010@qq.com.ORCID http://orcid.org/0000-0002-1623-5969

Funding

National Natural Science Foundation of China (National Science Foundation of China) No. 82060243
6 · The paper itself

Abstract

Neonatal hypoxic-ischemic encephalopathy (HIE) is worsened by autophagy-induced neuronal damage, with SYNPO2 playing a key role in this process. This study investigates the involvement of SYNPO2 in neuronal autophagy and explores the potential of bone marrow mesenchymal stem cells (BMSCs) to alleviate HIE-induced dysfunction by inhibiting SYNPO2-mediated autophagy. Using in vitro and in vivo neonatal HIE models, we observed an upregulation of SYNPO2 expression, accompanied by increased neuronal injury and aggregation of autophagy-related proteins. Intervention with BMSCs effectively reduced SYNPO2 expression, and SYNPO2 depression mitigated neuroautophagic damage and improved neurological dysfunctions. Moreover, SYNPO2 overexpression exacerbated neuroautophagy despite BMSC treatment, while SYNPO2 depletion notably reduced neuroautophagic damage and alleviated cognitive impairments, retaining the neuroprotective efficacy of BMSC treatment. These findings confirm the role of BMSCs in attenuating HIE injury by suppressing neuroautophagy and provide insights into the mechanistic involvement of SYNPO2. Ultimately, this study identifies SYNPO2 as a novel therapeutic target for neonatal HIE and supports the clinical potential of BMSCs in HIE management.

Indexed as

AutophagyHypoxia-Ischemia, BrainMesenchymal Stem CellsMesenchymal Stem Cell TransplantationAnimalsAnimals, NewbornDisease Models, AnimalDown-RegulationMaleNeuronsRatsRats, Sprague-Dawley

Identifiers

PMID40000609
PMCPMC11862179

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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.