Evidence map›Paper›PMID 26064438›Full record

ArticleAmerican journal of translational research2015

VEGF-C/VEGFR-3 pathway promotes myocyte hypertrophy and survival in the infarcted myocardium.

Tieqiang Zhao, Wenyuan Zhao, Weixin Meng, Chang Liu, Yuanjian Chen, Ivan C Gerling, Karl T Weber, Syamal K Bhattacharya, Rahul Kumar, Yao Sun

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2015. 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
1.4field-weighted citation impact, top 19% 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, 33 citations in OpenAlex.

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  12. CD146, from a melanoma cell adhesion molecule to a signaling receptor.Signal transduction and targeted therapy · 2020
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  14. Increased expression of vascular endothelial growth factor-C and vascular endothelial growth factor receptor-3 after pilocarpine-induced status epilepticus in mice.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019
    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

10 authors at 1 institution in 1 country.

Tieqiang ZhaoDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center Memphis, TN 38163, USA.
Wenyuan ZhaoDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center Memphis, TN 38163, USA.
Weixin MengDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center Memphis, TN 38163, USA.
Chang LiuDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center Memphis, TN 38163, USA.
Yuanjian ChenDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center Memphis, TN 38163, USA.
Ivan C GerlingDivision of Endocrinology, Department of Medicine, University of Tennessee Health Science Center Memphis, TN 38163, USA.
Karl T WeberDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center Memphis, TN 38163, USA.
Syamal K BhattacharyaDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center Memphis, TN 38163, USA.
Rahul KumarDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center Memphis, TN 38163, USA.
Yao SunDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center Memphis, TN 38163, USA.
University of Tennessee Health Science Center · US

Funding

Regulatory Mechanisms of Oxidative Stress in Cardiac Angiogenesis PostinfarctionR01HL096503 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SUN, YAO · 2010 to 2013
$1.5M
NHLBI NIH HHS R01 HL096503
6 · The paper itself

Abstract

backgroundNumerous studies have shown that in addition to angio/lymphangiogenesis, the VEGF family is involved in other cellular actions. We have recently reported that enhanced VEGF-C and VEGFR-3 in the infarcted rat myocardium, suggesting the paracrine/autocrine function of VEGF-C on cardiac remodeling. The current study was designed to test the hypothesis that VEGF-C regulates cardiomyocyte growth and survival in the infarcted myocardium. METHODS AND

resultsGene profiling and VEGFR-3 expression of cardiomyocytes were assessed by laser capture microdissection/microarray and immunohistochemistry in the normal and infarcted myocardium. The effect of VEGF-C on myocyte hypertrophy and apoptosis during normoxia and hypoxia was detected by RT-PCR and western blotting in cultured rat neonatal cardiomyocytes. VEGFR-3 was minimally expressed in cardiomyocytes of the normal and noninfarcted myocardium, while markedly elevated in the surviving cardiomyocytes of the infarcted myocardium and border zone. Genes altered in the surviving cardiomyocytes were associated with the networks regulating cellular growth and survival. VEGF-C significantly increased the expression of atrial natriuretic factor (ANP), brain natriuretic factor (BNP), and β-myosin heavy chain (MHC), markers of hypertrophy, in neonatal cardiomyocytes. Hypoxia caused neonatal cardiomyocyte atrophy, which was prevented by VEGF-C treatment. Hypoxia significantly enhanced apoptotic mediators, including cleaved caspase 3, 8, and 9, and Bax in neonatal cardiomyocytes, which were abolished by VEGF-C treatment.

conclusionOur findings indicate that VEGF-C/VEGFR-3 pathway exerts a beneficial role in the infarcted myocardium by promoting compensatory cardiomyocyte hypertrophy and survival.

Indexed as

apoptosiscardiomyocyteshypertrophymyocardial infarctionVEGF-C

Identifiers

PMID26064438
PMCPMC4455345
OpenAlexW2386933374

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.