Evidence map›Paper›PMID 27830026›Full record

ArticleAmerican journal of translational research2016

Puerarin inhibits cardiac fibrosis via monocyte chemoattractant protein (MCP)-1 and the transforming growth factor-β1 (TGF-β1) pathway in myocardial infarction mice.

Zhiwen Tao, Yingbin Ge, Ningtian Zhou, Yunle Wang, Weili Cheng, Zhijian Yang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  11. Monocyte recruitment and fate specification after myocardial infarction.American journal of physiology. Cell physiology · 2020
    Review
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  15. Article
  16. Diabetes and Cardioplegia.Journal of nature and science · 2017
    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 2 institutions in 1 country.

Zhiwen TaoDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029, Jiangsu Province, China; Department of Cardiology, Sir Run Run Hospital Nanjing Medical UniversityNanjing 211166, Jiangsu Province, China.
Yingbin GeDepartment of Physiology, Nanjing Medical University Nanjing 211166, Jiangsu Province, China.
Ningtian ZhouDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, Jiangsu Province, China.
Yunle WangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, Jiangsu Province, China.
Weili ChengDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, Jiangsu Province, China.
Zhijian YangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, Jiangsu Province, China.
Nanjing Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-β1 (TGF-β1) and inflammation play important roles in the cardiac fibrosis development associated with myocardial infarction (MI). Puerarin is wildly used for treatment of diabetes, cardiovascular disease and cerebrovascular disease in China, and recently some studies have shown its anti-cardiac fibrotic effect on myocardial hypertrophy. The purpose of our study was to determine whether puerarin has an anti-cardiac fibrotic effect after MI and find the potential mechanism. A mouse model of MI was established by standard LAD coronary artery ligation, and cardiac fibrosis was confirmed by Masson's staining and the expression of collagen I, III and α-SMA. The expression level of F4/80 (macrophage/monocyte marker in mouse), monocyte chemoattractant protein (MCP)-1 and TGF-β1 in cardiac tissue treated with or without puerarin was evaluated by immunohistochemistry analysis, enzyme-linked immunosorbent assay (ELISA) and quantitative polymerase chain reaction (qPCR). The downstream protein phospho-Smad (small mother against decapentaplegic) 2/3 was evaluated by westernblot. The results displayed that puerarin could inhibit the recruitment and activation of monocytes/macrophages, decrease the expression of TGF-β1 in the cardiac tissues, and consequently significantly attenuated cardiac fibrosis after MI. Our results also displayed a strong positive correlation between MCP-1 and TGF-β1 expression in MI. Thus, this study revealed the mechanism by which prevented cardiac fibrosis after MI through a decrease in MCP-1 expression and an inhibition TGF-β1 pathway, and indicated puerarin could be a potential agent in attenuating MI-induced cardiac fibrosis.

Indexed as

cardiac fibrosismonocyte chemoattractant protein (MCP-1)myocardial infarction (MI)Puerarintransforming growth factor-β1 (TGF-β1)

Identifiers

PMID27830026
PMCPMC5095335
OpenAlexW2560679522

What OpenQuestion holds

Textmetadata
Read underepoch 390

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 OpenQuestion graph.