Evidence map›Paper›PMID 40272647›Full record

ArticleCurrent medical science2025

Association of Decreased Fecal Microbiota Akkermansia with Increased High-Sensitivity C-Reactive Protein Levels in Patients with Unstable Angina.

Yuan-Fan Yuan, Ji-Yu Zhang, Jia-Hao Xu, Xin-Yi Xia, Miao Yu, Ling-Feng Zha, De-Sheng Hu, Wei-Min Wang, Chao-Long Wang, Qing Wang and 4 more

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Article in Current medical science, 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

14 authors.

Yuan-Fan Yuan *Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Ji-Yu Zhang *Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Jia-Hao XuDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Xin-Yi XiaDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Miao YuDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Ling-Feng ZhaDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
De-Sheng HuDepartment of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Wei-Min WangDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Chao-Long WangDepartment of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Qing WangKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, 430030, China.
Chen ChenDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Zhi-Lei ShanDepartment of Nutrition and Food Hygiene, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Fen YangDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. 2019xh0187@hust.edu.cn.ORCID http://orcid.org/0000-0002-1970-3270
Xiang ChengDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. nathancx@hust.edu.cn.ORCID http://orcid.org/0000-0002-6287-3128

Funding

the National Natural Science Foundation of China 82030016the National Natural Science Foundation of China 82200533the National Natural Science Foundation of China 82230011
6 · The paper itself

Abstract

BACKGROUND AND

objectiveInflammation plays a pivotal role in the progression of coronary artery disease (CAD). High-sensitivity C-reactive protein (hsCRP) serves as a well-established biomarker for assessing cardiovascular inflammation risk. However, the specific intestinal microbiota alteration contributing to increased inflammation remains unclear. Therefore, the present study investigated the correlation between the intestinal microbiota and inflammation in patients with unstable angina (UA).

methodsA cohort of 92 patients with UA was recruited for this study. The plasma hsCRP level was measured via a CardioPhase hsCRP assay, fecal samples were collected after admission, and 16S rRNA sequencing was conducted to identify the fecal microbial profile. The participants were classified into two groups according to the median hsCRP level (1.11 mg/L). The composition of the fecal microbiota was compared between patients with hsCRP ≥ 1.11 mg/L and those with hsCRP < 1.11 mg/L. Additionally, the correlations between the fecal microbiota and clinical characteristics were analyzed.

resultsA notable reduction in the relative abundance of Akkermansia was observed in patients with hsCRP ≥ 1.11 mg/L, whereas the diversity of the fecal microbiota was not significantly different between patients with hsCRP ≥ 1.11 mg/L and those with hsCRP < 1.11 mg/L. Furthermore, the abundance of Akkermansia was negatively correlated with hsCRP levels.

conclusionThis study suggested a significant association between decreased levels of Akkermansia and inflammatory risk in patients with UA. These findings underscore the potential role of the intestinal microbiota in contributing to inflammation in UA patients. Further work is needed on the mechanism by which the microbiota contributes to inflammatory risk.

Indexed as

AkkermansiaAngina, UnstableC-Reactive ProteinFecesGastrointestinal MicrobiomeAgedBiomarkersFemaleHumansInflammationMaleMiddle AgedRNA, Ribosomal, 16SBiomarkersC-Reactive ProteinRNA, Ribosomal, 16SAkkermansiaFecal microbiotaHigh-sensitivity C-reactive proteinInflammation riskUnstable angina

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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.