Evidence map›Paper›PMID 18556571›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2008

Murine models of hyperhomocysteinemia and their vascular phenotypes.

Sanjana Dayal, Steven R Lentz

Abstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
  2. Article
  3. Pathophysiology of homocysteine: insights into ion channel dysfunction.Pflugers Archiv : European journal of physiology · 2026
    Review
  4. Article
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  13. Apolipoprotein E ε4/4 genotype limits response to dietary induction of hyperhomocysteinemia and resulting inflammatory signaling.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    Article
  14. Review
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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

2 authors at 1 institution in 1 country.

Sanjana DayalDepartment of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, USA.
Steven R Lentz
University of Iowa · US

Funding

Transgenic and knockout animalP01NS024621 · NINDS · UNIVERSITY OF IOWA · PI SANFORD, L PHILLIP · 1987 to 2012
$14.9M
Vascular Mechanisms in Homocysteinemia and AtherosclerosisR01HL063943 · NHLBI · UNIVERSITY OF IOWA · PI LENTZ, STEVEN R · 2000 to 2012
$4.0M
NHLBI NIH HHS HL63943NHLBI NIH HHS R01 HL063943NINDS NIH HHS NS24621NINDS NIH HHS P01 NS024621
6 · The paper itself

Abstract

Hyperhomocysteinemia is an established risk factor for arterial as well as venous thromboembolism. Individuals with severe hyperhomocysteinemia caused by inherited genetic defects in homocysteine metabolism have an extremely high incidence of vascular thrombosis unless they are treated aggressively with homocysteine-lowering therapy. The clinical value of homocysteine-lowering therapy in individuals with moderate hyperhomocysteinemia, which is very common in populations at risk for vascular disease, is more controversial. Considerable progress in our understanding of the molecular mechanisms underlying the association between hyperhomocysteinemia and vascular thrombotic events has been provided by the development of a variety of murine models. Because levels of homocysteine are regulated by both the methionine and folate cycles, hyperhomocysteinemia can be induced in mice through both genetic and dietary manipulations. Mice deficient in the cystathionine beta-synthase (CBS) gene have been exploited widely in many studies investigating the vascular pathophysiology of hyperhomocysteinemia. In this article, we review the established murine models, including the CBS-deficient mouse as well as several newer murine models available for the study of hyperhomocysteinemia. We also summarize the major vascular phenotypes observed in these murine models.

Indexed as

AnimalsBetaine-Homocysteine S-MethyltransferaseDietDisease Models, AnimalEndothelium, VascularEnzyme InhibitorsGenetic Predisposition to DiseaseHomocysteineHyperhomocysteinemiaMicePhenotypeThrombosisBetaine-Homocysteine S-MethyltransferaseBhmt protein, mouseEnzyme InhibitorsHomocysteine

Identifiers

PMID18556571
PMCPMC2574668
OpenAlexW2025945219

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.