Evidence map›Paper›PMID 39419946›Full record

ArticleCardiovascular toxicology2024

Protective Role of (-)-Epicatechin on Trimethylamine-N-Oxide (TMAO)-Induced Cardiac Hypertrophy via SP1/SIRT1/SUMO1 Signaling Pathway.

Siting Hong, Jing Lu, Jiaoyan Li, Yingchun Luo, Dongxue Liu, Yuanyuan Jin, Zeng Wang, Yibo Wang, Hao Zhang, Xin Zhang and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Siting HongDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Jing LuThe Key Laboratory of Cardiovascular Disease Acousto-Optic Electromagnetic Diagnosis and Treatment in Heilongjiang Province, the First Affiliated Hospital, Harbin Medical University, Harbin, China.
Jiaoyan LiDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Yingchun LuoDepartment of Pharmacology (The Key Laboratory of Cardiovascular Research, Ministry of Education) at College of Pharmacy, Harbin Medical University, Harbin, China.
Dongxue LiuDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Yuanyuan JinDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Zeng WangDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Yibo WangDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Hao ZhangCollege of Clinical Medicine, North China University of Science and Technology, Tangshan, Hebei, China.
Xin ZhangDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Yang LiDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Haoruo ZhangDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Zengxiang DongThe Key Laboratory of Cardiovascular Disease Acousto-Optic Electromagnetic Diagnosis and Treatment in Heilongjiang Province, the First Affiliated Hospital, Harbin Medical University, Harbin, China.
Zhaojun WangDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China. hyd2013@qq.com.
Lin LvExperimental Animal Center, First Affiliated Hospital, Harbin Medical University, Harbin, China. dicklin1992@163.com.
Zhaoguang LiangDepartment of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China. zhaoguangliangsupper@126.com.

Funding

National Natural Science Foundation of China 81870169National Natural Science Foundation of China 82000297the Doctor Funds of the First Affiliated Hospital of Harbin Medical University 2019B09the Postdoctoral Research Fund of China 2018M631963the Support Project for Outstanding Young Talents of the First Affiliated Hospital of Harbin Medical University 2024YQ15
6 · The paper itself

Abstract

(-)-Epicatechin (EPI) is beneficial for cardiovascular health. Trimethylamine N-oxide (TMAO), a gut microbe-derived food metabolite, is strongly associated with the risk of cardiovascular diseases. However, the effects and underlying mechanisms of EPI on TMAO-induced cardiac hypertrophy remain unclear. This study aimed to determine whether EPI inhibits TMAO-induced cardiac hypertrophy. Plasma levels of TMAO in control participants and patients with cardiac hypertrophy were measured and analyzed. Male C57BL/6 mice were randomly divided into control group, TMAO group, EPI group and TMAO + EPI group. According to the groups assignments, mice received intraperitoneal (i.p.) injection of normal saline or i.p. injection of TMAO (150 mg/kg/day) for 14 days. The EPI group was given intragastric (i.g.) administration of EPI alone (1 mg/kg/day) for 21 days, and TMAO + EPI group received i.g. administration of EPI for 7 days before starting i.p. injection of TMAO, continuing until the end of the TMAO treatment. Histological analyses of the mice's hearts was accessed by H&E and Masson staining. In vitro, H9c2 cells were induced to hypertrophy by TMAO (10 µM) for 24 h and were pre-treated with or without EPI (10 µM) for 1 h. Protein level of cardiac hypertrophy markers and Sp1/SIRT1/SUMO1 pathway were determined by western blot. The plasma level of TMAO was 2.66 ± 1.59 μmol/L in patients with cardiac hypertrophy and 0.62 ± 0.30 μmol/L in control participants. EPI attenuated TMAO-induced hypertrophy in H9c2 cells. In vivo, TMAO induced cardiac hypertrophy and impaired the cardiac function of mice. Pathological staining showed that TMAO induced cardiac hypertrophy and collagen deposition in mice. EPI treatment improved the cardiac function, inhibited the myocardial hypertrophy induced by TMAO. EPI significantly attenuated the TMAO-induced upregulation of ANP and BNP and the downregulation of SP1, SIRT1 and SUMO1 in vivo and in vitro. EPI may suppress TMAO-induced cardiac hypertrophy by activating the Sp1/SIRT1/SUMO1 signaling pathway.

Indexed as

CatechinDisease Models, AnimalMethylaminesMice, Inbred C57BLMyocytes, CardiacSignal TransductionSirtuin 1Sp1 Transcription FactorAnimalsCardiomegalyCase-Control StudiesCell LineFemaleHumansHypertrophy, Left VentricularMaleCatechinMethylaminesSIRT1 protein, humanSirt1 protein, mouseSirtuin 1SP1 protein, humanSp1 Transcription FactortrimethyloxamineCardiac hypertrophy(-)-EpicatechinSP1/SIRT1/SUMO1Trimethylamine N-oxide

Identifiers

PMID39419946
PMCPMC11564365

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.