Evidence map›Paper›PMID 40595567›Full record

ArticleNature communications2025

Connexin43 hemichannel blockade turns microglia neuroprotective and mitigates cognitive deficits in a mouse model of amyloidosis.

Yixun Su, Hui Li, Wenjie Zhang, Shi Tao, Qi Wang, Xuan Zhang, Mi Zhou, Xiaomin Huang, Chenmeng Wang, Yong Tang and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Astrocytic KFrontiers in aging neuroscience · 2026
    Review
  11. Article
  12. Article
  13. Review
  14. The Src inhibitor peptide TAT-Cx43Neuro-oncology advances
    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.

Yixun SuResearch Centre, Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.ORCID http://orcid.org/0000-0001-8215-4270
Hui LiResearch Centre, Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.
Wenjie ZhangSchool of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Shi TaoSchool of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Qi WangResearch Centre, Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.
Xuan ZhangSchool of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Mi ZhouDepartment of Central Laboratory, Qianjiang Hospital, Chongqing University, Qianjiang, Chongqing, China.
Xiaomin HuangResearch Centre, Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.
Chenmeng WangResearch Centre, Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.ORCID http://orcid.org/0009-0007-8273-5201
Yong TangInternational Joint Research Centre on Purinergic Signalling/School of Health and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu, China.ORCID http://orcid.org/0000-0002-2543-066X
Hui ChenSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Ultimo, Australia.ORCID http://orcid.org/0000-0001-6883-3752
Alexei VerkhratskyFaculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.ORCID http://orcid.org/0000-0003-2592-9898
Zhengbao ZhaSchool of Food and Biological Engineering, Hefei University of Technology, Hefei, China. zbzha@hfut.edu.cn.ORCID http://orcid.org/0000-0003-3646-4969
Jianqin NiuDepartment of Histology and Embryology, Third Military Medical University, Chongqing, China. jianqinniu@tmmu.edu.cn.
Chenju YiResearch Centre, Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China. yichj@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-8686-4525

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32170980National Natural Science Foundation of China (National Science Foundation of China) 32271034
6 · The paper itself

Abstract

Alzheimer's disease (AD), the leading cause of senile dementia, lacks effective therapies. While microglia are central to AD pathology, key therapeutic targets remain unclear. Here we identify microglial connexin43 (Cx43) hemichannels as a regulator of microglial reactivity in AD, positioning them as a promising therapeutic target. Post-mortem AD patient tissue showed elevated Cx43 levels in periplaque microglia. In the APP

Indexed as

Alzheimer DiseaseAmyloidosisCognitive DysfunctionConnexin 43MicrogliaAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalFemaleHumansMaleMiceMice, KnockoutMice, TransgenicNeuroprotectionAmyloid beta-PeptidesAmyloid beta-Protein PrecursorConnexin 43GJA1 protein, mousePresenilin-1

Identifiers

PMID40595567
PMCPMC12219535

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.