Evidence map›Paper›PMID 28193718›Full record

ArticleCirculation. Heart failure2017

H-Ras Isoform Mediates Protection Against Pressure Overload-Induced Cardiac Dysfunction in Part Through Activation of AKT.

Takahisa Matsuda, Jae Im Jeong, Shohei Ikeda, Takanobu Yamamoto, Shumin Gao, Gopal J Babu, Peiyong Zhai, Dominic P Del Re

Open access · bronzeAbstract read
In one paragraph

Article in Circulation. Heart failure, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Takahisa MatsudaFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine, Rutgers, New Jersey Medical School, Newark, NJ.
Jae Im JeongFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine, Rutgers, New Jersey Medical School, Newark, NJ.
Shohei IkedaFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine, Rutgers, New Jersey Medical School, Newark, NJ.
Takanobu YamamotoFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine, Rutgers, New Jersey Medical School, Newark, NJ.
Shumin GaoFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine, Rutgers, New Jersey Medical School, Newark, NJ.
Gopal J BabuFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine, Rutgers, New Jersey Medical School, Newark, NJ.
Peiyong ZhaiFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine, Rutgers, New Jersey Medical School, Newark, NJ.
Dominic P Del ReFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine, Rutgers, New Jersey Medical School, Newark, NJ. delredo@njms.rutgers.edu.
Rutgers, The State University of New Jersey · US

Funding

The role of NF2 in myocardial ischemia and reperfusion injuryR01HL127339 · NHLBI · RBHS-NEW JERSEY MEDICAL SCHOOL · PI DEL RE, DOMINIC P · 2015 to 2019
$2.0M
The role of RASSF1A in myocardial ischemia/reperfusion injuryR21HL122669 · NHLBI · RBHS-NEW JERSEY MEDICAL SCHOOL · PI DEL RE, DOMINIC P · 2013 to 2013
$159k
NHLBI NIH HHS R01 HL127339NHLBI NIH HHS R21 HL122669
6 · The paper itself

Abstract

backgroundIn general, Ras proteins are thought to promote cardiac hypertrophy, an important risk factor for cardiovascular disease and heart failure. However, the contribution of different Ras isoforms has not been investigated. The objective of this study was to define the role of H- and K-Ras in modulating stress-induced myocardial hypertrophy and failure. METHODS AND

resultsWe used H- and K-Ras gene knockout mice and subjected them to pressure overload to induce cardiac hypertrophy and dysfunction. We observed a worsened cardiac phenotype in

conclusionsTaken together, these findings indicate that H- and K-Ras have divergent effects on cardiac hypertrophy and heart failure in response to pressure overload stress.

Indexed as

Arterial PressureAnimalsAnimals, NewbornAorta, ThoracicCardiomegalyCells, CulturedDisease Models, AnimalEnzyme ActivationGenotypeHeart FailureLigationMaleMice, KnockoutMyocytes, CardiacOncogene ProteinsPhenotypeHras protein, mouseHras protein, ratOncogene ProteinsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)ras Proteinscardiomyocytesheart failurehypertensionhypertrophyRas proteins

Identifiers

PMID28193718
PMCPMC5325037
OpenAlexW2765972236

What OpenQuestion holds

Textmetadata
LicenceTDM
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.