Evidence map›Paper›PMID 10377171›Full record

ArticleThe Journal of clinical investigation1999

Genetics of Cd36 and the clustering of multiple cardiovascular risk factors in spontaneous hypertension.

M Pravenec, V Zidek, M Simakova, V Kren, D Krenova, K Horky, M Jachymova, B Mikova, L Kazdova, T J Aitman and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
8.7field-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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
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  6. Downregulation of theAntioxidants (Basel, Switzerland) · 2020
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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

17 authors at 7 institutions in 3 countries.

M PravenecInstitute of Physiology, Czech Academy of Sciences, Prague.
V Zidek
M Simakova
V Kren
D Krenova
K Horky
M Jachymova
B Mikova
L Kazdova
T J Aitman
P C Churchill
R C Webb
N H Hingarh
Y Yang
J M Wang
E M Lezin
T W Kurtz
University of California, San Francisco · USCharles University · CZCzech Academy of Sciences, Institute of Physiology · CZHammersmith Hospital · GBInstitute of Clinical and Experimental Medicine · CZUniversity of Michigan–Ann Arbor · USWayne State University · US

Funding

UNIQUE CARDIOVASCULAR RESPONSE TO STRESSORS AND LINKAGE WITH HYPERTENSIONP01HL035018 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PRINTZ, MORTON P · 1986 to 2007
$14.7M
VASCULAR GLUCOSE TRANSPORTERS IN HYPERTENSIONP01HL018575 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GREKIN, ROGER J · 1985 to 2003
$5.5M
NEW EXPERIMENTAL MODELS OF HYPERTENSIONR01HL056028 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KURTZ, THEODORE W · 1997 to 2012
$4.0M
NHLBI NIH HHS HL-18575NHLBI NIH HHS P01 HL018575NHLBI NIH HHS P01 HL035018NHLBI NIH HHS P01 HL-35018NHLBI NIH HHS R01 HL056028NHLBI NIH HHS R01 HL-56028
6 · The paper itself

Abstract

Disorders of carbohydrate and lipid metabolism have been reported to cluster in patients with essential hypertension and in spontaneously hypertensive rats (SHRs). A deletion in the Cd36 gene on chromosome 4 has recently been implicated in defective carbohydrate and lipid metabolism in isolated adipocytes from SHRs. However, the role of Cd36 and chromosome 4 in the control of blood pressure and systemic cardiovascular risk factors in SHRs is unknown. In the SHR. BN-Il6/Npy congenic strain, we have found that transfer of a segment of chromosome 4 (including Cd36) from the Brown Norway (BN) rat onto the SHR background induces reductions in blood pressure and ameliorates dietary-induced glucose intolerance, hyperinsulinemia, and hypertriglyceridemia. These results demonstrate that a single chromosome region can influence a broad spectrum of cardiovascular risk factors involved in the hypertension metabolic syndrome. However, analysis of Cd36 genotypes in the SHR and stroke-prone SHR strains indicates that the deletion variant of Cd36 was not critical to the initial selection for hypertension in the SHR model. Thus, the ability of chromosome 4 to influence multiple cardiovascular risk factors, including hypertension, may depend on linkage of Cd36 to other genes trapped within the differential segment of the SHR. BN-Il6/Npy strain.

Indexed as

AnimalsAnimals, CongenicBlood GlucoseCD36 AntigensCerebrovascular DisordersCluster AnalysisGenotypeHemodynamicsHypertensionInsulinLipidsPhenotypeRatsRats, Inbred BNRats, Inbred SHRRisk FactorsBlood GlucoseCD36 AntigensInsulinLipids

Identifiers

PMID10377171
PMCPMC408390
OpenAlexW2004237513

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.