Evidence map›Paper›PMID 23878601›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2013

Regulation of DDAH1 as a Potential Therapeutic Target for Treating Cardiovascular Diseases.

Xiaoyu Liu, John Fassett, Yidong Wei, Yingjie Chen

Open access · hybridAbstract read
In one paragraph

Article in Evidence-based complementary and alternative medicine : eCAM, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Immune and Metabolic Mechanisms of Endothelial Dysfunction.International journal of molecular sciences · 2024
    Review
  5. Review
  6. Article
  7. Review
  8. Dimethylarginine dimethylaminohydrolase 1 protects PMParticle and fibre toxicology · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Jornal vascular brasileiro
    Review
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

4 authors at 3 institutions in 2 countries.

Xiaoyu LiuShanghai Tenth People's Hospital, Tongji University, Shanghai, China.
John Fassett
Yidong Wei
Yingjie Chen
Shanghai Tenth People's Hospital · CNMinneapolis Heart Institute Foundation · USUniversity of Minnesota · US

Funding

MYOCARDIAL PERFUSION IN THE HYPERTROPHIED HEARTR01HL021872 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BACHE, ROBERT JAMES · 1985 to 2010
$3.7M
Translational Control in IPFR01HL089249 · NHLBI · UNIVERSITY OF MINNESOTA · PI BITTERMAN, PETER B · 2008 to 2011
$1.8M
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
NHLBI NIH HHS R01 HL021872NHLBI NIH HHS R01 HL089249NHLBI NIH HHS R01 HL105406NHLBI NIH HHS R21 HL098669NHLBI NIH HHS R21 HL098719NHLBI NIH HHS R21 HL102597
6 · The paper itself

Abstract

Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor that blocks nitric oxide production, while congestive heart failure is associated with increased plasma and tissue ADMA content. Increased plasma ADMA is a strong and independent predictor of all-cause mortality in the community and the strongest predictor of mortality in patients after myocardial infarction. Recent studies demonstrated that dimethylarginine dimethylaminohydrolase-1 (DDAH1) is the critical enzyme for ADMA degradation and thereby plays an important role in maintaining cardiovascular nitric oxide bioavailability. Interestingly, activation of the farnesoid X receptor (FXR) through the bile acid ursodeoxycholic acid (UDCA) or synthetic FXR agonists, such as GW4064, can increase DDAH1 expression. Thus, modulating DDAH1 activity through FXR receptor agonists such as UDCA could be a therapeutic target for treating reduced nitric oxide bioavailability in congestive heart failure and other cardiovascular diseases.

Identifiers

PMID23878601
PMCPMC3710625
OpenAlexW2117078485

What OpenQuestion holds

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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.