Evidence map›Paper›PMID 38616256›Full record

ArticleJournal of cardiothoracic surgery2024

Mechanism of sodium butyrate, a metabolite of gut microbiota, regulating cardiac fibroblast transdifferentiation via the NLRP3/Caspase-1 pyroptosis pathway.

Tiancheng Dong, Dingkao Huang, Zhengzheng Jin

Open access · goldAbstract read
In one paragraph

Article in Journal of cardiothoracic surgery, 2024. 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
1.2field-weighted citation impact, top 23% of its field
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, 5 citations in OpenAlex.

  1. Article
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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

3 authors at 1 institution in 1 country.

Tiancheng DongDepartment of Intensive care unit, Wenzhou TCM Hospital of Zhejiang Chinese Medical University, No. 9 Liuhongqiao Jiaowei Road, Wenzhou City, 325000, Zhejiang Province, China.
Dingkao HuangDepartment of Intensive care unit, Wenzhou TCM Hospital of Zhejiang Chinese Medical University, No. 9 Liuhongqiao Jiaowei Road, Wenzhou City, 325000, Zhejiang Province, China.
Zhengzheng JinDepartment of Intensive care unit, Wenzhou TCM Hospital of Zhejiang Chinese Medical University, No. 9 Liuhongqiao Jiaowei Road, Wenzhou City, 325000, Zhejiang Province, China. Zzjin_wz@163.com.
Zhejiang Chinese Medical University · CN

Funding

Study on the Effect of Trimethylamine N-oxid on Myocardial Fibrosis by Regulating the NOX/ROS Signal Pathway and Promoting endothelial-to-mesenchymal transition Y20220498
6 · The paper itself

Abstract

backgroundCardiac fibroblasts (CFs) are activated after initial injury, and then differentiate into myofibroblasts (MFs), which play a pivotal role as the primary mediator cells in pathological remodeling. Sodium butyrate (NaB), being a metabolite of gut microbiota, exhibits anti-inflammatory property in local therapies on sites other than the intestine. Thus, this study aimed to probe the mechanism by which NaB regulates CFs transdifferentiation through the NLRP3/Caspase-1 pyroptosis pathway.

methodsCFs were cultured in vitro and induced into MFs by TGFβ1. CFs were identified by immunofluorescence labelling technique of vimentin and α-SMA, followed by treatment with NaB or NLRP3 inflammasome inhibitor (CY-09) and its activator [nigericin sodium salt (NSS)]. The expression levels of α-SMA, GSDMD-N/NLRP3/cleaved Caspase-1 proteins, and inflammatory factors IL-1β/IL-18/IL-6/IL-10 were determined using immunofluorescence, Western blot and ELISA. Cell proliferation and migration were evaluated using the CCK-8 assay and the cell scratch test, respectively.

resultsFollowing the induction of TGFβ1, CFs exhibited increased expression levels of α-SMA proteins and IL-6/IL-10, as well as cell proliferative and migratory abilities. TGFβ1 induced CFs to differentiate into MFs, while NaB inhibited this differentiation. NaB inactivated the NLRP3/Caspase-1 pyroptosis pathway. CY-09 demonstrated inhibitory effects on the NLRP3/Caspase-1 pyroptosis pathway, leading to a reduction in TGFβ1-induced CFs transdifferentiation. NSS activated the NLRP3/Caspase-1 pyroptosis pathway, and thus partially counteracting the inhibitory effect of intestinal microbiota metabolite NaB on CFs transdifferentiation.

conclusionNaB, a metabolite of the gut microbiota, inhibited the activation of the NLRP3/Caspase-1 pyroptosis pathway in TGFβ1-induced CFs, repressed the transdifferentiation of CFs into MFs.

Indexed as

Gastrointestinal MicrobiomeButyric AcidCaspase 1Cell TransdifferentiationFibroblastsHumansInterleukin-10Interleukin-6NLR Family, Pyrin Domain-Containing 3 ProteinPyroptosisButyric AcidCaspase 1Interleukin-10Interleukin-6NLR Family, Pyrin Domain-Containing 3 ProteinCardiac fibroblastsCaspase-1Cell pyroptosisGut microbiota metabolite sodium butyrateMyofibroblastsNLRP3 inflammasomesTGFβ1α-SMA

Identifiers

PMID38616256
PMCPMC11017590
OpenAlexW4394796606

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.