Evidence map›Paper›PMID 39227800›Full record

ArticleBMC medicine2024

Hyperactivation of ATF4/TGF-β1 signaling contributes to the progressive cardiac fibrosis in Arrhythmogenic cardiomyopathy caused by DSG2 Variant.

Baowei Zhang, Yizhang Wu, Chunjiang Zhou, Jiaxi Xie, Youming Zhang, Xingbo Yang, Jing Xiao, Dao Wu Wang, Congjia Shan, Xiujuan Zhou and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

12 authors.

Baowei Zhang *Department of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, 150 Jimo Road, Pudong, Shanghai, 200120, P.R. China.
Yizhang Wu *Department of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, 150 Jimo Road, Pudong, Shanghai, 200120, P.R. China.
Chunjiang ZhouDepartment of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, 150 Jimo Road, Pudong, Shanghai, 200120, P.R. China.
Jiaxi XieDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, P.R. China.
Youming ZhangDepartment of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, 150 Jimo Road, Pudong, Shanghai, 200120, P.R. China.
Xingbo YangShanghai East Hospital, School of Life Sciences and Technology, Tongji University, 150 Jimo Road, Pudong, Shanghai, 200120, P.R. China.
Jing XiaoShanghai East Hospital, School of Life Sciences and Technology, Tongji University, 150 Jimo Road, Pudong, Shanghai, 200120, P.R. China.
Dao Wu WangState Key Laboratory of Reproductive Medicine, the Centre for Clinical Reproductive Medicine, Department of Cardiology, the First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, P.R. China.
Congjia ShanModel Animal Research Center, Nanjing University, Nanjing, China.
Xiujuan ZhouDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, P.R. China.
Yaozu XiangShanghai East Hospital, School of Life Sciences and Technology, Tongji University, 150 Jimo Road, Pudong, Shanghai, 200120, P.R. China. yaozu.xiang@tongji.edu.cn.
Bing YangDepartment of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, 150 Jimo Road, Pudong, Shanghai, 200120, P.R. China. bingyang@tongji.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundArrhythmogenic cardiomyopathy (ACM) is an inherited cardiomyopathy characterized with progressive cardiac fibrosis and heart failure. However, the exact mechanism driving the progression of cardiac fibrosis and heart failure in ACM remains elusive. This study aims to investigate the underlying mechanisms of progressive cardiac fibrosis in ACM caused by newly identified Desmoglein-2 (DSG2) variation.

methodsWe identified homozygous DSG2

resultsAll eight patients with ACM were homozygous for DSG2

conclusionsHyperactivation of the ATF4/TGF-β1 signaling in cardiomyocytes emerges as a novel mechanism underlying progressive cardiac fibrosis in ACM. Targeting the ATF4/TGF-β1 signaling may be a novel therapeutic target for managing ACM.

Indexed as

Activating Transcription Factor 4Desmoglein 2FibrosisSignal TransductionTransforming Growth Factor beta1AdultAnimalsArrhythmogenic Right Ventricular DysplasiaFemaleHumansMaleMiceMiddle AgedMyocytes, CardiacPedigreeActivating Transcription Factor 4ATF4 protein, humanAtf4 protein, mouseDesmoglein 2DSG2 protein, humanDsg2 protein, mouseTransforming Growth Factor beta1Activating transcription factor 4Arrhythmogenic cardiomyopathyCardiac fibrosisDesmoglein 2Transforming growth factor β1

Identifiers

PMID39227800
PMCPMC11373413

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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.