Evidence map›Paper›PMID 23130158›Full record

ArticleJournal of the American Heart Association2012

CaMK4 Gene Deletion Induces Hypertension.

Gaetano Santulli, Ersilia Cipolletta, Daniela Sorriento, Carmine Del Giudice, Antonio Anastasio, Sara Monaco, Angela Serena Maione, Gianluigi Condorelli, Annibale Puca, Bruno Trimarco and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 4 pooled it
17.7field-weighted citation impact, top 1% 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

117 citing papers in PubMed, 4 syntheses or guidelines pooled it, 211 citations in OpenAlex.

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  16. A Retinoic Acid ReceptorThe Journal of pharmacology and experimental therapeutics · 2021
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57 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 1 country.

Gaetano SantulliDepartment of Clinical Medicine, Cardiovascular and Immunologic Sciences, "Federico II" University of Naples, Naples, Italy (G.S., E.C., D.S., C.D.G., A.A., B.T.).
Ersilia Cipolletta
Daniela Sorriento
Carmine Del Giudice
Antonio Anastasio
Sara Monaco
Angela Serena Maione
Gianluigi Condorelli
Annibale Puca
Bruno Trimarco
Maddalena Illario
Guido Iaccarino
University of Naples Federico II · ITMultiMedica · ITIstituto Ortopedico Gaetano Pini · ITUniversity of Salerno · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe expression of calcium/calmodulin-dependent kinase IV (CaMKIV) was hitherto thought to be confined to the nervous system. However, a recent genome-wide analysis indicated an association between hypertension and a single-nucleotide polymorphism (rs10491334) of the human CaMKIV gene (CaMK4), which suggests a role for this kinase in the regulation of vascular tone. METHODS AND

resultsTo directly assess the role of CaMKIV in hypertension, we characterized the cardiovascular phenotype of CaMK4(-/-) mice. They displayed a typical hypertensive phenotype, including high blood pressure levels, cardiac hypertrophy, vascular and kidney damage, and reduced tolerance to chronic ischemia and myocardial infarction compared with wild-type littermates. Interestingly, in vitro experiments showed the ability of this kinase to activate endothelial nitric oxide synthase. Eventually, in a population study, we found that the rs10491334 variant associates with a reduction in the expression levels of CaMKIV in lymphocytes from hypertensive patients.

conclusionsTaken together, our results provide evidence that CaMKIV plays a pivotal role in blood pressure regulation through the control of endothelial nitric oxide synthase activity. (J Am Heart Assoc. 2012;1:e001081 doi: 10.1161/JAHA.112.001081.).

Indexed as

angiogenesisarrhythmiaendotheliumhypertensionhypertrophy

Identifiers

PMID23130158
PMCPMC3487344
OpenAlexW2161571281

What OpenQuestion holds

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LicenceCC BY
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.