Evidence map›Paper›PMID 38951640›Full record

ArticleCommunications biology2024

PEX3 promotes regenerative repair after myocardial injury in mice through facilitating plasma membrane localization of ITGB3.

Jia-Teng Sun, Zi-Mu Wang, Liu-Hua Zhou, Tong-Tong Yang, Di Zhao, Yu-Lin Bao, Si-Bo Wang, Ling-Feng Gu, Jia-Wen Chen, Tian-Kai Shan and 11 more

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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  5. Review
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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

21 authors.

Jia-Teng Sun *Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Zi-Mu Wang *Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Liu-Hua Zhou *Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Tong-Tong Yang *Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Di ZhaoDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Yu-Lin BaoDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Si-Bo WangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.ORCID 0000-0002-3204-2710
Ling-Feng GuDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.ORCID 0000-0003-0021-4722
Jia-Wen ChenDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Tian-Kai ShanDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Tian-Wen WeiDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Hao WangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Qi-Ming WangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Xiang-Qing KongDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Li-Ping XieKey Laboratory of Cardiovascular and Cerebrovascular Medicine, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Ai-Hua GuState Key Laboratory of Reproductive Medicine, School of Public Health, Nanjing Medical University, Nanjing, China.
Yang ZhaoDepartment of Biostatistics, School of Public Health, China International Cooperation Center for Environment and Human Health, Nanjing Medical University, Nanjing, 210029, China.
Feng ChenDepartment of Biostatistics, School of Public Health, China International Cooperation Center for Environment and Human Health, Nanjing Medical University, Nanjing, 210029, China.
Yong JiKey Laboratory of Cardiovascular and Cerebrovascular Medicine, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.ORCID 0000-0003-2650-5747
Yi-Qiang CuiState Key Laboratory of Reproductive Medicine, Department of Histology and Embryology, Nanjing Medical University, Nanjing, 210029, China. cuiyiqiang@126.com.
Lian-Sheng WangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China. drlswang@njmu.edu.cn.ORCID 0000-0001-8538-6560

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The peroxisome is a versatile organelle that performs diverse metabolic functions. PEX3, a critical regulator of the peroxisome, participates in various biological processes associated with the peroxisome. Whether PEX3 is involved in peroxisome-related redox homeostasis and myocardial regenerative repair remains elusive. We investigate that cardiomyocyte-specific PEX3 knockout (Pex3-KO) results in an imbalance of redox homeostasis and disrupts the endogenous proliferation/development at different times and spatial locations. Using Pex3-KO mice and myocardium-targeted intervention approaches, the effects of PEX3 on myocardial regenerative repair during both physiological and pathological stages are explored. Mechanistically, lipid metabolomics reveals that PEX3 promotes myocardial regenerative repair by affecting plasmalogen metabolism. Further, we find that PEX3-regulated plasmalogen activates the AKT/GSK3β signaling pathway via the plasma membrane localization of ITGB3. Our study indicates that PEX3 may represent a novel therapeutic target for myocardial regenerative repair following injury.

Indexed as

Cell MembraneIntegrin beta3Mice, KnockoutRegenerationAnimalsCell ProliferationHeart InjuriesLipoproteinsMaleMembrane ProteinsMiceMice, Inbred C57BLMyocardiumMyocytes, CardiacPlasmalogensSignal TransductionIntegrin beta3Itgb3 protein, mouseLipoproteinsMembrane ProteinsPEX3 protein, mousePlasmalogens

Identifiers

PMID38951640
PMCPMC11217276

What OpenQuestion holds

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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.