Evidence map›Paper›PMID 41126379›Full record

ArticleBiomarker research2025

Proteomic and histopathologic profiling reveal molecular features and clinical biomarkers of coronary atherosclerosis.

Xinjie Xu, Zhongli Chen, Sifei Chen, Jiansong Huang, Jiali Chen, Jiaying Cao, Hang Gao, Enhao Huang, Yibo Zhang, Xiangjie Li and 9 more

Abstract readLetter
In one paragraph

Article in Biomarker research, 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

19 authors.

Xinjie Xu *State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Zhongli Chen *State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Sifei ChenState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Jiansong HuangThe First School of Clinical Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jiali ChenThe Second School of Clinical Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Jiaying CaoThe First School of Clinical Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Hang GaoState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Enhao HuangState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Yibo ZhangState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Xiangjie LiState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Yifeng ZhangDepartment of Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaorui LiuState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Shengkang HuangState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Ke YangDepartment of Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yang YangState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Wenjia ZhangState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Ying SongState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Liang ChenState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China. liang.chen9@hotmail.com.
Zhan HuState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China. huzhan@fuwai.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular features of coronary atherosclerosis progression remain incompletely understood. A comprehensive characterization of coronary proteome dynamics during atherosclerosis progression could facilitate the identification of novel biomarkers for early detection of plaque initiation and risk assessment of plaque destabilization. We performed proteomics on human coronary artery specimens representing five progressive histopathologic stages of atherosclerosis according to the modified AHA classification, including adaptive intimal thickening (AIT), pathological intimal thickening (PIT), fibroatheroma (FA), thin cap fibroatheroma (TCFA), and ruptured plaque (RP). The results revealed progressive dysregulation of complement and coagulation cascades and extracellular matrix (ECM) organization during histopathologic progression, particularly in plaque initiation and destabilization. Integrated single-cell RNA sequencing data showed that complement and coagulation pathways were predominantly upregulated in fibroblasts and macrophages, while ECM organization was elevated in fibroblasts and smooth muscle cells. Plasma proteomics in a discovery cohort identified THBS1, ECM2, and C1R proteins as robust diagnostic biomarkers from among the overlapping complement and ECM proteins found in the tissue proteomics. The combination of these biomarkers achieved area under the curve (AUC) values of 0.831 in the training set and 0.764 in the test set for identifying coronary artery disease (CAD). In both the discovery cohort and the external validation cohort, this biomarker panel distinguished stable CAD from non-stenosis controls (AUC: 0.765 and 0.841, respectively) and identified ACS patients (AUC: 0.786 and 0.822, respectively). These findings elucidate the proteomic landscape of atherosclerosis progression and establish a three-protein biomarker panel with potential for CAD diagnosis.

Indexed as

AtherosclerosisBiomarkerHistopathologic classificationHuman coronary arteryProteomics

Identifiers

PMID41126379
PMCPMC12548267

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.