Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Correlation of a common mutation in the methylenetetrahydrofolate reductase gene with plasma homocysteine in patients with premature coronary artery disease.

Arteriosclerosis, thrombosis, and vascular biology - 1 Mar 1997

Christensen B, Frosst P, Lussier-Cacan S, Selhub J, Goyette P, Rosenblatt D S, Genest J, Rozen R

Abstract excerpt

Mild hyperhomocysteinemia, a risk factor for occlusive arterial disease, can be caused by disruptions of homocysteine metabolism. Methylenetetrahydrofolate reductase (MTHFR) catalyzes the synthesis of 5-methyltetrahydrofolate, the methyl donor for homocysteine remethylation to methionine. A common mutation in MTHFR, an alanine-to-valine substitution, may contribute to mild hyperhomocysteinemia in coronary artery...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Coronary Disease
Share to CAD gene

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to MTHFR gene

Share to Homocysteine

Share to Methylenetetrahydrofolate Reductase (NADPH2)

Share to Mutation

Share to Oxidoreductases Acting on CH-NH Group Donors

Source

Identifiers

PMID: 9102178
DOI: 10.1161/01.atv.17.3.569

Genes

CAD
MTHFR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Correlation of a common mutation in the methylenetetrahydrofolate reductase gene with plasma homocysteine in patients with premature coronary artery disease.PMID 9102178Read ↗

Methylenetetrahydrofolate reductase C677T mutation, plasma homocysteine, and folate in subjects from northern Italy with or without angiographically documented severe coronary atherosclerotic disease: evidence for an important genetic-environmental interaction.Semantic proximity Read ↗

Common mutation in methylenetetrahydrofolate reductase. Correlation with homocysteine metabolism and late-onset vascular disease.Semantic proximity Read ↗

Thermolabile methylenetetrahydrofolate reductase in coronary artery disease.Semantic proximity Read ↗

Common mutation in methylenetetrahydrofolate reductase. Correlation with homocysteine and other risk factors for vascular disease.Semantic proximity Read ↗

Homocysteine and risk of premature coronary heart disease. Evidence for a common gene mutation.Semantic proximity Read ↗

Association of polymorphism in the thermolabile 5, 10-methylene tetrahydrofolate reductase gene and hyperhomocysteinemia with coronary artery disease.Semantic proximity Read ↗

Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations.Semantic proximity Read ↗

Genetic causes of mild hyperhomocysteinemia in patients with premature occlusive coronary artery diseases.Semantic proximity Read ↗

Correlation between C677T MTHFR gene polymorphism, plasma homocysteine levels and the incidence of CAD.Semantic proximity Read ↗

Methylenetetrahydrofolate reductase gene and coronary artery disease.Semantic proximity Read ↗

The 677C-->T mutation in the methylenetetrahydrofolate reductase gene: associations with plasma total homocysteine levels and risk of coronary atherosclerotic disease.Semantic proximity Read ↗

Common methylenetetrahydrofolate reductase gene mutation leads to hyperhomocysteinemia but not to vascular disease: the result of a meta-analysis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.