Evidence map›Paper›PMID 10683374›Full record

ArticleThe Journal of clinical investigation2000

Enhanced atherosclerosis and kidney dysfunction in eNOS(-/-)Apoe(-/-) mice are ameliorated by enalapril treatment.

J W Knowles, R L Reddick, J C Jennette, E G Shesely, O Smithies, N Maeda

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
10.8field-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

87 citing papers in PubMed, 301 citations in OpenAlex.

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  19. AMPK: Potential Therapeutic Target for Vascular Calcification.Frontiers in cardiovascular medicine · 2021
    Review
  20. The role of TRPV1 channels in atherosclerosis.Channels (Austin, Tex.) · 2020
    Review

27 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

6 authors at 4 institutions in 1 country.

J W KnowlesDepartment of Pathology, Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
R L Reddick
J C Jennette
E G Shesely
O Smithies
N Maeda
Emory University Hospital · USHenry Ford Health System · USThe University of Texas Health Science Center at San Antonio · USUniversity of North Carolina at Chapel Hill · US

Funding

MODELS FOR STUDYING THE GENETICS OF HYPERTENSIONR01HL049277 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1992 to 2025
$17.5M
APOLIPOROTEIN GENES AND ATHEROGENESISR01HL042630 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1989 to 2017
$4.9M
APOLIPOPROTEIN GENES AND ATHEROGENESIS IN ANIMALSR37HL042630 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1998 to 2007
$3.4M
GENETIC INTERACTIONS IN ATHEROSCLEROSIS AND HYPERTENSIONR01HL062845 · NHLBI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1999 to 2002
$759k
NHLBI NIH HHS HL-42630NHLBI NIH HHS HL-49277NHLBI NIH HHS HL-62845NHLBI NIH HHS R01 HL042630NHLBI NIH HHS R01 HL049277NHLBI NIH HHS R37 HL042630
6 · The paper itself

Abstract

Hypertension and atherosclerosis are each important causes of morbidity and mortality in the developed world. We have investigated the interaction between these conditions by breeding mice that are atherosclerotic due to lack of apolipoprotein (apo) E with mice that are hypertensive due to lack of endothelial nitric oxide synthase (eNOS). The doubly deficient mice (nnee) have higher blood pressure (BP) and increased atherosclerotic lesion size but no change in plasma lipoprotein profiles compared with normotensive but atherosclerotic (NNee) mice. The nnee mice also develop kidney damage, evidenced by increased plasma creatinine, decreased kidney weight/body weight ratio, and glomerular lipid deposition and calcification. Enalapril treatment abolishes the deleterious effects of eNOS deficiency on BP, atherosclerosis, and kidney dysfunction in nnee mice. In striking contrast, a genetic lack of inducible NOS, which does not affect BP, has no effect on the development of atherosclerotic lesions in Apoe(-/-) mice. We also observed a positive relationship between BP and size of atherosclerotic lesions These results suggest that the atherogenic effects of eNOS deficiency can be partially explained by an increase in BP and reemphasize the importance of controlling hypertension in preventing atherosclerosis.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAnimalsAntihypertensive AgentsApolipoproteins EArteriosclerosisBlood PressureEnalaprilHypertensionKidney DiseasesMiceMice, Mutant StrainsNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIOrgan SizeAngiotensin-Converting Enzyme InhibitorsAntihypertensive AgentsApolipoproteins EEnalaprilNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos2 protein, mouseNos3 protein, mouse

Identifiers

PMID10683374
PMCPMC289160
OpenAlexW2091430270

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.