Evidence map›Paper›PMID 35135471›Full record

ArticleMolecular medicine (Cambridge, Mass.)2022

Gut bacterial metabolite Urolithin A inhibits myocardial fibrosis through activation of Nrf2 pathway in vitro and in vivo.

Pengfei Chen, Junyu Pei, Xiaopu Wang, Shi Tai, Liang Tang, Xinqun Hu

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  5. Signaling Pathways and Therapeutic Approaches in Post-Myocardial Infarction Fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2025
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  16. Raspberry polyphenols target molecular pathways of heart failure.The Journal of nutritional biochemistry · 2024
    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

6 authors at 1 institution in 1 country.

Pengfei ChenDepartment of Cardiology, The Second Xiangya Hospital of Central South University, No.139, Middle Ren-min Road, Changsha, 410011, Hunan Province, People's Republic of China.
Junyu PeiDepartment of Cardiology, The Second Xiangya Hospital of Central South University, No.139, Middle Ren-min Road, Changsha, 410011, Hunan Province, People's Republic of China.
Xiaopu WangDepartment of Cardiology, The Second Xiangya Hospital of Central South University, No.139, Middle Ren-min Road, Changsha, 410011, Hunan Province, People's Republic of China.
Shi TaiDepartment of Cardiology, The Second Xiangya Hospital of Central South University, No.139, Middle Ren-min Road, Changsha, 410011, Hunan Province, People's Republic of China.
Liang TangDepartment of Cardiology, The Second Xiangya Hospital of Central South University, No.139, Middle Ren-min Road, Changsha, 410011, Hunan Province, People's Republic of China.
Xinqun HuDepartment of Cardiology, The Second Xiangya Hospital of Central South University, No.139, Middle Ren-min Road, Changsha, 410011, Hunan Province, People's Republic of China. hxqsci@csu.edu.cn.ORCID 0000-0002-4154-7972
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial fibrosis after myocardial infarction (MI) is one of the leading causes of cardiovascular diseases. Cardiac fibroblasts (CFs) are activated and promoted by MI to undergo myofibroblast transformation (CMT). Urolithin A (UA) is an active and effective gut metabolite derived from polyphenolics of berries and pomegranate fruits, which has been reported to have anti-inflammatory and anti-oxidant functions. However, whether UA affects the CMT process during myocardial fibrosis remains unclear.

methodsTGF-β1-treated primary rat cardiac fibroblasts were used for in vitro study. Cell proliferation ability was evaluated by MTT assay. Cell migration and invasion abilities were tested by wound healing and Transwell assays. The expression of CMT process-related markers were measured by qRT-PCR and western blot. The rat MI model was established by left anterior descending coronary artery (LAD) ligation and evaluated by H&E and Masson staining.

resultsOur data demonstrated that UA treatment could inhibit the CMT process in TGF-β1-induced CFs, including cell proliferation, migration and invasion abilities. Knocking down of Nrf2, which was activated by UA treatment, could mitigate the effects of UA treatment on CMT process. Moreover, in vivo administration of UA in rat MI model successfully up-regulated Nrf2 expression and improved the myocardial damage and fibrosis.

conclusionsThe study discovered the function and mechanism of UA on myocardial fibrosis and demonstrated the protective effects of UA administration through activation of Nrf2 pathway.

Indexed as

Gastrointestinal MicrobiomeAnimalsBiomarkersCell MovementCell ProliferationCoumarinsFibrosisMyocardial InfarctionMyocardiumMyofibroblastsNF-E2-Related Factor 2RatsSignal Transduction3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-oneBiomarkersCoumarinsNF-E2-Related Factor 2Myocardial fibrosisMyofibroblast transformationNrf2Urolithin A

Identifiers

PMID35135471
PMCPMC8822684
OpenAlexW4210825402

What OpenQuestion holds

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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.