Evidence map›Paper›PMID 40612272›Full record

ArticleCell insight2025

TFAP4 exacerbates pathological cardiac fibrosis by modulating mechanotransduction.

Jie Liu, Jingjing Feng, Jingxuan Zhao, Xiangjie Kong, Zhangyi Yu, Yuanru Huang, Zechun He, Mengxin Liu, Zheng Liu, Zhibing Lu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell insight, 2025. 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. Review
  2. 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

11 authors.

Jie LiuDepartment of Cardiology, Zhongnan Hospital of Wuhan University, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan 430071, Hubei, China.
Jingjing FengThe Institute for Advanced Studies, TaiKang Center for Life and Medical Sciences, Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan 430072, Hubei , China.
Jingxuan ZhaoDepartment of Cardiology, Zhongnan Hospital of Wuhan University, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan 430071, Hubei, China.
Xiangjie KongDepartment of Cardiology, Zhongnan Hospital of Wuhan University, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan 430071, Hubei, China.
Zhangyi YuDepartment of Cardiology, Zhongnan Hospital of Wuhan University, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan 430071, Hubei, China.
Yuanru HuangDepartment of Cardiology, Zhongnan Hospital of Wuhan University, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan 430071, Hubei, China.
Zechun HeDepartment of Cardiology, Zhongnan Hospital of Wuhan University, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan 430071, Hubei, China.
Mengxin LiuDepartment of Cardiology, Zhongnan Hospital of Wuhan University, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan 430071, Hubei, China.
Zheng LiuThe Institute for Advanced Studies, TaiKang Center for Life and Medical Sciences, Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan 430072, Hubei , China.
Zhibing LuDepartment of Cardiology, Zhongnan Hospital of Wuhan University, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan 430071, Hubei, China.
Li WangDepartment of Cardiology, Zhongnan Hospital of Wuhan University, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan 430071, Hubei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac fibroblast (CF) differentiation into myofibroblasts is a crucial driver of cardiac fibrosis, leading to extensive extracellular matrix (ECM) deposition that increases myocardial stiffness and eventually impairs heart function. Mechanotransduction has merged as a key regulator of CF activation and the fibrotic response post-myocardial infarction (MI). However, the molecular mechanisms linking CF activation to mechanical cues within the injured myocardium remain poorly understood. Here we identified transcription factor TFAP4 as a central regulator of fibrosis in both human and murine models. TFAP4 overexpression enhances CF proliferation, ECM protein expression, and myofibroblast differentiation. Notably, TFAP4 directly activates expression of mechanosensors including Itga11 and Piezo2, which are essential for transmitting mechanical signals that promote CF activation and fibrosis. Silencing

Indexed as

Cardiac fibrosisFibroblast activationMechanotransductionTFAP4

Identifiers

PMID40612272
PMCPMC12226091

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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.