Evidence mapPaperPMID 41076121Full record

ArticleJournal of advanced research2026

Bacteroides vulgatus alleviates heart failure via butyric acid-TGF-β1/MAPK pathway.

Zhiyong Du, Wenxin Zhang, Yu Wang, Xinlan Fang, Yifan Zhang, Yuling Xiao, Xiangrui Zeng, Shuo Yuan, Yong Jiang, Xiaoyu Guo and 6 more

Abstract read
In one paragraph

Article in Journal of advanced research, 2026. 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. The gut microbiota: an emerging therapeutic target for ICI-associated myocarditis.Frontiers in cellular and infection microbiology · 2026
    Review
  3. 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

16 authors.

Zhiyong DuBeijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Disease, Beijing, China.
Wenxin ZhangState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China.
Yu WangBeijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Disease, Beijing, China.
Xinlan FangState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China.
Yifan ZhangState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China.
Yuling XiaoState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China.
Xiangrui ZengState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China.
Shuo YuanState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China.
Yong JiangState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China.
Xiaoyu GuoState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China.
Kun HuaBeijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Disease, Beijing, China.
Xiubin YangBeijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Disease, Beijing, China.
Xuedong ZhaoBeijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Disease, Beijing, China. Electronic address: zxdd1@126.com.
Yuhua LiuBeijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Disease, Beijing, China. Electronic address: lyh951025@126.com.
Yingyuan LuState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China. Electronic address: luyingyuan518@bjmu.edu.cn.
Pengfei TuState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China. Electronic address: pengfeitu@bjmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe gut microbiota plays a vital role in the progression of heart failure (HF), making it a potential strategy for treating HF. The Bacteroides genus has shown promising potential for treating HF. However, further research is needed to identify specific beneficial Bacteroides strains for treating HF and elucidate their potential mechanisms.

objectivesThis study aimed to elucidate the therapeutic effect and mechanism of Bacteroides strain on HF.

methodsThis study comprehensively used pharmacological evaluation, 16S rRNA genetic sequencing, short-chain fatty acid (SCFA) targeted metabolomics, transcriptome, and molecular biology methods to investigate the efficacy and mechanism of Bacteroides vulgatus (B. vulgatus) in the treatment of HF.

resultsWe observed a significant decrease in the abundance of B. vulgatus in both HF patients and mice, and dysbiosis of the gut microbiota could cause cardiac dysfunction in mice. The administration of B. vulgatus to mice with HF significantly improved their cardiac function and significantly increased the levels of SCFAs, especially butyric acid. Meanwhile, we also observed a significant reduction in the level of butyric acid in the serum of HF patients, and the cardiac function of HF mice improved after the administration of butyric acid. Compared to patients with higher butyric acid level, patients with lower butyric acid level had a significantly increased incidence of endpoint events. Moreover, the transcriptome results revealed that B. vulgatus significantly regulated the mitogen-activated protein kinase (MAPK) pathway. After further molecular biology verification, B. vulgatus was confirmed to regulate the transforming growth factor-β1 (TGF-β1)/MAPK pathway in the heart through butyric acid, thereby exerting anti-HF effects.

conclusionThis study provides evidence that B. vulgatus improves heart function by regulating SCFA metabolism and subsequently modulating the TGF-β1/MAPK pathway in myocardial tissue, confirming the potential therapeutic role of B. vulgatus in HF.

Indexed as

BacteroidesButyric AcidHeart FailureMAP Kinase Signaling SystemTransforming Growth Factor beta1AnimalsDisease Models, AnimalFatty Acids, VolatileFemaleGastrointestinal MicrobiomeHumansMaleMiceMice, Inbred C57BLRNA, Ribosomal, 16SButyric AcidFatty Acids, VolatileRNA, Ribosomal, 16STransforming Growth Factor beta1Bacteroides vulgatusButyric acidHeart failure (HF)Short-chain fatty acid (SCFA) metabolismTGF-β1/MAPK pathway

Identifiers

PMID41076121
PMCPMC13227243

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.