Evidence map›Paper›PMID 39611812›Full record

ArticlemSystems2025

Multi-omics mechanical analysis of gut microbiota, carboxylic acids, and cardiac gene expression interaction triggering diabetic cardiomyopathy.

Meixin Shi, Bingbing Zhao, Wenjie Cai, Hui Yuan, Xiao Liang, Zhitao Li, Xinyu Liu, Ye Jin, Xi Liu, Can Wei

Erratum issuedAbstract read
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Article in mSystems, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Illuminating diabetesWorld journal of diabetes · 2025
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Meixin Shi *Department of Pathophysiology, Harbin Medical University, Harbin, Heilongjiang, China.
Bingbing Zhao *Department of Pathophysiology, Harbin Medical University, Harbin, Heilongjiang, China.
Wenjie Cai *Department of Pathophysiology, Harbin Medical University, Harbin, Heilongjiang, China.
Hui Yuan *School of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang, Heilongjiang, China.
Xiao Liang *Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Zhitao LiDepartment of Pathophysiology, Harbin Medical University, Harbin, Heilongjiang, China.
Xinyu LiuSchool of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang, Heilongjiang, China.
Ye JinDepartment of General Surgery, Key Laboratory of Hepatosplenic Surgery, Ministry of Education, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0009-0003-6646-2240
Xi LiuDepartment of Cardiology, Ordos Central Hospital, Ordos, China.ORCID 0009-0007-3587-820X
Can WeiDepartment of General Surgery, Key Laboratory of Hepatosplenic Surgery, Ministry of Education, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0003-4291-7653

Funding

MOST | National Natural Science Foundation of China (NSFC) 82170268,82200482
6 · The paper itself

Abstract

It is well known that gut microbial imbalance is a potential factor for the occurrence and development of diabetes mellitus (DM) and its complications. Moreover, the heart and gut microbiota can regulate each other through the gut-metabolite-heart axis. In this study, metagenomics, metabolomics, and transcriptomics were chosen to sequence the changes in gut microbiota, serum metabolite levels, and differentially expressed genes (DEGs) in leptin receptor-deficient db/db mice and analyze the correlation between serum metabolites and gut microbiota or DEGs. According to the results, there were significant differences in the 1,029 cardiac genes and 353 serum metabolites in diabetic mice of the db/db group, including DEGs enriched in the PPAR signaling pathway and increased short-chain carboxylic acids (CAs), when compared with the normal db/m group. According to metagenomics, the gut microbiota of mice in the db/db group were disrupted, and particularly Lachnospiraceae bacteria and Oscillospiraceae bacteria significantly decreased. Also, according to the Pearson correlation analysis, a significant positive correlation was found between CAs and PPAR signaling pathway-related DEGs, and a negative correlation was found between CAs and the abundance of the above-mentioned species. To sum up, type 2 diabetes mellitus (T2DM) can upregulate the expression of partial cardiac genes through the levels of serum short-chain CAs affected by gut microbiota, thus playing a role in the occurrence and development of diabetic cardiomyopathy (DCM). IMPORTANCE: Our research results clearly link the changes in heart genes of T2DM and normal mice with changes in serum metabolites and gut microbiota, indicating that some genes in biological processes are closely related to the reduction of protective microbiota in the gut microbiota. This study provides a theoretical basis for investigating the mechanism of DCM and may provide preliminary evidence for the future use of gut microbiota therapy for DCM.

Indexed as

Carboxylic AcidsDiabetic CardiomyopathiesGastrointestinal MicrobiomeAnimalsDiabetes Mellitus, Type 2MaleMetabolomicsMetagenomicsMiceMice, Inbred C57BLMultiomicsMyocardiumTranscriptomeCarboxylic Acidscarboxylic acidsdiabetic cardiomyopathygut microbiotaPPAR signaling pathway

Identifiers

PMID39611812
PMCPMC11748484

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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.