Evidence map›Paper›PMID 40610735›Full record

ArticleCellular and molecular life sciences : CMLS2025

Cell division cycle protein 42-driven activation of the MKK3/6-p38 signaling pathway participates in cardiac remodeling in mice.

Ke Wen, Lin Xie, Quan-Wen Liu, Guan-Hui Yu, Xu-Hui Qiao, Yu-Chun Huang, Lu Wang, Xin Li, Li-Dan Wen, Xiao-Lei Wang and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. 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

16 authors.

Ke Wen *The National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Lin Xie *The National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Quan-Wen Liu *The National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Guan-Hui YuThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Xu-Hui QiaoThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Yu-Chun HuangThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Lu WangThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Xin LiThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Li-Dan WenThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Xiao-Lei WangThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Jing HeThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Xin-Yu XiaoThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Xiao-Xiao ZhaoThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Ling-Fang WangThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China.
Hong-Bo XinThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China. xinhb@ncu.edu.cn.
Ke-Yu DengThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, 330031, Nanchang, China. dky@ncu.edu.cn.ORCID http://orcid.org/0000-0002-3519-6846

Funding

Jiangxi Provincial Department of Science and Technology 20212BCJ23043Jiangxi Provincial Department of Science and Technology 20224BAB216015National Key Research and Development Program of China 2022YFA1104300National Natural Science Foundation of China 81970256, 81760140National Natural Science Foundation of China 82000354National Natural Science Foundation of China 82270302,82470454,81873659Science and technology project of Health Commission of Jiangxi Province 202410005
6 · The paper itself

Abstract

Cell division cycle protein 42 (Cdc42) is a member of the Rho GTPase subfamily that serves as a signal mediating factor in cell cycle division, cytoskeleton arrangement, cell polarization, membrane trafficking and signal transduction. However, the role of Cdc42 in cardiac remodeling, including hypertrophy and fibrosis, remains controversial. This study aimed to clarify the role and underlying mechanism of Cdc42 in cardiac remodeling. Cardiac Cdc42 knockout (Cdc42

Indexed as

Cardiomegalycdc42 GTP-Binding ProteinMAP Kinase Kinase 3MAP Kinase Kinase 6MAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesVentricular RemodelingAngiotensin IIAnimalsFibrosisMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumMyocytes, CardiacAngiotensin IIcdc42 GTP-Binding ProteinCdc42 protein, mouseMap2k3 protein, mouseMap2k6 protein, mouseMAP Kinase Kinase 3MAP Kinase Kinase 6p38 Mitogen-Activated Protein KinasesApoptosisCardiac functionCardiomyocyte hypertrophyInflammation

Identifiers

PMID40610735
PMCPMC12229389

What OpenQuestion 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 OpenQuestion graph.