Evidence map›Paper›PMID 40537817›Full record

ArticleClinical epigenetics2025

cfDNA methylation detection as potential liquid biopsy of multiple organ injury in myocarditis patients.

Yangchao Zhao, Yujia Wang, Xi Zhao, Xin Zhang, Haoyan Wang, Liang Cui, Huifen Wang, Weiwei Zhu, Boyan Li, Yanjun Zhou and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

22 authors.

Yangchao Zhao *Department of Extracorporeal Life Support Center, Department of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yujia Wang *Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xi Zhao *Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xin Zhang *Department of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Haoyan Wang *Geneplus-Beijing Institute, 9th Floor, No.6 Building, Peking University Medical Industrial Park, Zhongguancun Life Science Park, Beijing, China.
Liang Cui *Geneplus-Beijing Institute, 9th Floor, No.6 Building, Peking University Medical Industrial Park, Zhongguancun Life Science Park, Beijing, China.
Huifen WangGene Hospital of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Weiwei ZhuGene Hospital of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Boyan LiDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yanjun ZhouDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jun LiDepartment of Extracorporeal Life Support Center, Department of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Guowei FuDepartment of Extracorporeal Life Support Center, Department of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yiheng ZhouHenan Medical School of Zhengzhou University, Zhengzhou, China.
Pengwei SunDepartment of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jing BaiGeneplus-Beijing Institute, 9th Floor, No.6 Building, Peking University Medical Industrial Park, Zhongguancun Life Science Park, Beijing, China.
Xuefeng XiaGene Hospital of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xin YiGeneplus-Beijing Institute, 9th Floor, No.6 Building, Peking University Medical Industrial Park, Zhongguancun Life Science Park, Beijing, China.
Ling YangGeneplus-Beijing Institute, 9th Floor, No.6 Building, Peking University Medical Industrial Park, Zhongguancun Life Science Park, Beijing, China.
Chaoqun ChenOrgan Procurement Organizations, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Junnan TangDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. fcctangjn@zzu.edu.cn.
Ang LiGene Hospital of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. lia@zju.edu.cn.
Zujiang YuGene Hospital of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. johnyuem@zzu.edu.cn.

Funding

Fund of infectious diseases Detection and Tumor Targeted Therapy Engineering Research Center of Henan Province 112696High throughput sequencing technology in infectious diseases MTP2022A007
6 · The paper itself

Abstract

Myocarditis is inflammatory injury of the myocardium and causes approximately 30,000 deaths globally each year. Fulminant myocarditis is an extremely severe form of myocarditis. Currently, the clinical evaluation of myocarditis and fulminant myocarditis is primarily based on symptoms, ECG findings, and biochemical markers. Cardiac magnetic resonance and endomyocardial biopsy can provide further support for the diagnosis, but both have limitations in routine practice. Recent studies have shown that cell-free DNA (cfDNA) has distinct methylation patterns depending on the organ of origin, suggesting new possibilities for tracking specific types of organ damage. The core mechanism of fulminant myocarditis is a cytokine storm, leading to multiorgan damage, differing from clinically suspected myocarditis. We performed Genome-wide cfDNA methylation detection on plasma from 20 healthy donors and 22 patients (fulminant myocarditis: clinically suspected myocarditis = 9:13, COVID-19 positive: COVID-19 negative = 14:8) and found that cfDNA can be used to specifically identify early multiorgan damage caused by fulminant myocarditis, and its AUC is superior to traditional biochemical indicators such as troponin, high-sensitivity troponin, and lactate dehydrogenase. This is critically important for the timely clinical recognition and treatment of this condition. Furthermore, our study findings suggest that SARS-CoV-2 infection may exacerbate the severity of myocarditis and multiorgan damage. In summary, cfDNA shows great potential as a noninvasive, early, and sensitive biomarker for reflecting disease severity and systemic injury in fulminant myocarditis, which may help guide earlier risk stratification and intervention.

Indexed as

Cell-Free Nucleic AcidsCOVID-19DNA MethylationMyocarditisAdultBiomarkersCase-Control StudiesFemaleHumansLiquid BiopsyMaleMiddle AgedSARS-CoV-2BiomarkersCell-Free Nucleic AcidsCell-free DNACytokine stormEarly identificationFulminant myocarditisMultiorgan damage

Identifiers

PMID40537817
PMCPMC12180197

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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.