Evidence map›Paper›PMID 37722560›Full record

ArticleJournal of advanced research2024

Deciphering mechanisms of cardiomyocytes and non-cardiomyocyte transformation in myocardial remodeling of permanent atrial fibrillation.

Yixuan Sheng, Yin-Ying Wang, Yuan Chang, Dongting Ye, Liying Wu, Hongen Kang, Xiong Zhang, Xiao Chen, Bin Li, Daliang Zhu and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Single-Nucleus RNA Sequencing Reveals SPP1Journal of cardiovascular development and disease · 2026
    Article
  6. Article
  7. Review
  8. Metabolic and Inflammatory Mechanisms Driving Atrial Fibrillation.Annual review of pharmacology and toxicology · 2026
    Review
  9. Article
  10. Article
  11. Impact of Sorbs2 dysfunction on cardiovascular diseases.Biochimica et biophysica acta. Molecular basis of disease · 2025
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

16 authors.

Yixuan ShengDepartment of Cardiovascular Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China; State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, 167A Beilishi Road, Xi Cheng District, Beijing 100037, China.
Yin-Ying WangCAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences and China National Center for Bioinformation, Beijing, China.
Yuan ChangBeijing Key Laboratory of Preclinical Research and Evaluation for Cardiovascular Implant Materials, Animal Experimental Centre, Fuwai Hospital, National Centre for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China; State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, 167A Beilishi Road, Xi Cheng District, Beijing 100037, China.
Dongting YeDepartment of Cardiovascular Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Liying WuDepartment of Cardiovascular Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Hongen KangCAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences and China National Center for Bioinformation, Beijing, China; University of Chinese Academy of Sciences, Beijing, China.
Xiong ZhangDepartment of Cardiovascular Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Xiao ChenBeijing Key Laboratory of Preclinical Research and Evaluation for Cardiovascular Implant Materials, Animal Experimental Centre, Fuwai Hospital, National Centre for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China; State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, 167A Beilishi Road, Xi Cheng District, Beijing 100037, China.
Bin LiDepartment of Cardiovascular Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Daliang ZhuDepartment of Cardiovascular Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Ningning ZhangBeijing Key Laboratory of Preclinical Research and Evaluation for Cardiovascular Implant Materials, Animal Experimental Centre, Fuwai Hospital, National Centre for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China; Beijing Key Laboratory of Preclinical Research and Evaluation for Cardiovascular Implant Materials, Animal Experimental Centre, Fuwai Hospital, National Centre for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.
Haisen ZhaoDepartment of Cardiovascular Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Aijun ChenDepartment of Cardiovascular Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Haisheng ChenDepartment of Cardiovascular Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China. Electronic address: Drchenhaisheng@163.com.
Peilin JiaCAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences and China National Center for Bioinformation, Beijing, China. Electronic address: pjia@big.ac.cn.
Jiangping SongShenzhen Key Laboratory of Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen 518057, China; Beijing Key Laboratory of Preclinical Research and Evaluation for Cardiovascular Implant Materials, Animal Experimental Centre, Fuwai Hospital, National Centre for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China; State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, 167A Beilishi Road, Xi Cheng District, Beijing 100037, China. Electronic address: fwsongjiangping@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAtrial fibrillation (AF) is the most prevalent cardiac arrhythmia, and it significantly increases the risk of cardiovascular complications and morbidity, even with appropriate treatment. Tissue remodeling has been a significant topic, while its systematic transcriptional signature remains unclear in AF.

objectivesOur study aims to systematically investigate the molecular characteristics of AF at the cellular-level.

methodsWe conducted single-nuclei RNA-sequencig (snRNA-seq) analysis using nuclei isolated from the left atrial appendage (LAA) of AF patients and sinus rhythm. Pathological staining was performed to validate the key findings of snRNA-seq.

resultsA total of 30 cell subtypes were identified among 80, 592 nuclei. Within the LAA of AF, we observed a specific subtype of dedifferentiated cardiomyocytes (CMs) characterized by reduced expression of cardiac contractile proteins (TTN and TRDN) and heightened expression of extracellular-matrix related genes (COL1A2 and FBN1). Transcription factor prediction analysis revealed that gene expression patterns in dedifferentiated CMs were primarily regulated by CEBPG and GISLI. Additionally, we identified a distinct subtype of endothelial progenitor cells (EPCs) demonstrating elevated expression of PROM1 and KDR, a population decreased within the LAA of AF. Epicardial adipocytes disclosed a reduced release of the anti-inflammatory and anti-fibrotic factor PRG4, and an augmented secretion of VEGF signals targeting CMs. Additionally, we noted accumulation of M2-like macrophages and CD8

conclusionsThis study has discovered the presence of dedifferentiated CMs, a decrease in endothelial progenitor cells, a shift in the secretion profile of adipocytes, and an amplified inflammatory response in AF. These findings could offer crucial insights for future research on AF and serve as valuable references for investigating novel therapeutic approaches for AF.

Indexed as

Atrial FibrillationMyocytes, CardiacAdipocytesAgedAtrial AppendageAtrial RemodelingFemaleHumansMaleMiddle AgedRNA, Small NuclearVentricular RemodelingRNA, Small NuclearAtrial fibrillationCardiomyocyte dedifferentiationEpicardial adipose tissueLeft atrial appendage remodelingSingle-nuclei RNA-sequencing

Identifiers

PMID37722560
PMCPMC11258668

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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.