Evidence map›Paper›PMID 21493890›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2011

Dimethylarginine dimethylaminohydrolase-1 is the critical enzyme for degrading the cardiovascular risk factor asymmetrical dimethylarginine.

Xinli Hu, Dorothee Atzler, Xin Xu, Ping Zhang, Haipeng Guo, Zhongbing Lu, John Fassett, Edzard Schwedhelm, Rainer H Böger, Robert J Bache and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 139 citations in OpenAlex.

  1. Review
  2. Article
  3. The Emerging Role of the DDAH Proteins in Psychiatric Disorders.Biological psychiatry global open science · 2025
    Review
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  15. Dimethylarginine dimethylaminohydrolase 1 protects PMParticle and fibre toxicology · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Xinli HuCardiovascular Division, Lillehei Heart Institute, University of Minnesota, Minneapolis, MN 55455, USA.
Dorothee Atzler
Xin Xu
Ping Zhang
Haipeng Guo
Zhongbing Lu
John Fassett
Edzard Schwedhelm
Rainer H Böger
Robert J Bache
Yingjie Chen
Universität Hamburg · DE

Funding

MYOCARDIAL PERFUSION IN THE HYPERTROPHIED HEARTR01HL021872 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BACHE, ROBERT JAMES · 1985 to 2010
$3.7M
THE CORONARY VASCULAR RESPONSE TO ISCHEMIAR01HL020598 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BACHE, ROBERT JAMES · 1985 to 2007
$1.9M
Molecular mechanism of 4E-binding proteins on heart failure developmentR01HL105406 · NHLBI · UNIVERSITY OF MINNESOTA · PI CHEN, YINGJIE · 2011 to 2014
$1.5M
DDAH1 effects on endogenous NOS inhibitors and vascular endothelial functionR21HL098669 · NHLBI · UNIVERSITY OF MINNESOTA · PI CHEN, YINGJIE · 2010 to 2011
$415k
Regulation of the novel mTOR suppressor DDIT4 in the failing heartR21HL098719 · NHLBI · UNIVERSITY OF MINNESOTA · PI CHEN, YINGJIE · 2011 to 2012
$415k
DDAH1 effects on the development of congestive heart failureR21HL102597 · NHLBI · UNIVERSITY OF MINNESOTA · PI CHEN, YINGJIE · 2010 to 2011
$415k
THE CORONARY VASCULAR RESPONSE TO ISCHEMIAR37HL020598 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BACHE, ROBERT JAMES · 1987 to 1996
–
NHLBI NIH HHS HL021872NHLBI NIH HHS HL20598NHLBI NIH HHS R01 HL020598NHLBI NIH HHS R01 HL021872NHLBI NIH HHS R01 HL105406NHLBI NIH HHS R21 HL098669NHLBI NIH HHS R21HL098669NHLBI NIH HHS R21 HL098719NHLBI NIH HHS R21HL098719NHLBI NIH HHS R21 HL102597NHLBI NIH HHS R21HL102597
6 · The paper itself

Abstract

objectiveThe objective of this study was to identify the role of dimethylarginine dimethylaminohydrolase-1 (DDAH1) in degrading the endogenous nitric oxide synthase inhibitors asymmetrical dimethylarginine (ADMA) and N(g)-monomethyl-L-arginine (L-NMMA). METHODS AND

resultsWe generated a global-DDAH1 gene-deficient (DDAH1(-/-)) mouse strain to examine the role of DDAH1 in ADMA and l-NMMA degradation and the physiological consequences of loss of DDAH1. Plasma and tissue ADMA and L-NMMA levels in DDAH1(-/-) mice were several folds higher than in wild-type mice, but growth and development of these DDAH1(-/-) mice were similar to those of their wild-type littermates. Although the expression of DDAH2 was unaffected, DDAH activity was undetectable in all tissues tested. These findings indicate that DDAH1 is the critical enzyme for ADMA and L-NMMA degradation. Blood pressure was ≈ 20 mm Hg higher in the DDAH1(-/-) mice than in wild-type mice, but no other cardiovascular phenotype was found under unstressed conditions. Crossing DDAH1(+/-) male with DDAH1(+/-) female mice yielded DDAH1(+/+), DDAH1(+/-), and DDAH1(-/-) mice at the anticipated ratio of 1:2:1, indicating that DDAH1 is not required for embryonic development in this strain.

conclusionsOur findings indicate that DDAH1 is required for metabolizing ADMA and L-NMMA in vivo, whereas DDAH2 had no detectable role for degrading ADMA and l-NMMA.

Indexed as

AmidohydrolasesAnimalsArginineBlood PressureCardiovascular DiseasesCells, CulturedEndothelial CellsEnzyme InhibitorsFemaleGenotypeHypertensionInfusion Pumps, ImplantableMaleMiceMice, 129 StrainMice, KnockoutAmidohydrolasesArgininedimethylargininaseEnzyme InhibitorsNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseN,N-dimethylarginineomega-N-Methylarginine

Identifiers

PMID21493890
PMCPMC3117037
OpenAlexW2112529329

What OpenQuestion holds

Textmetadata
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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.