ArticleJournal of medical genetics2006
The Pro279Leu variant in the transcription factor MEF2A is associated with myocardial infarction.
Article in Journal of medical genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Pooled it
- Myocyte Enhancer Factor-2A Gene Mutation and Coronary Artery Disease.Chinese medical journal · 2015Trial
- Myocyte Enhancer Factor 2A Plays a Central Role in the Regulatory Networks of Cellular Physiopathology.Aging and disease · 2023Review
- Article
- Variants in3 Biotech · 2018Article
- Shenfu Injection attenuates rat myocardial hypertrophy by up-regulating miR-19a-3p expression.Scientific reports · 2018Article
- Novel 6-bp deletion in MEF2A linked to premature coronary artery disease in a large Chinese family.Molecular medicine reports · 2016Article
- The canonical Wingless signaling pathway is required but not sufficient for inflow tract formation in the Drosophila melanogaster heart.Developmental biology · 2016Article
- Genetics of coronary artery disease and myocardial infarction.World journal of cardiology · 2016Review
- Article
- RNA interference of myocyte enhancer factor 2A accelerates atherosclerosis in apolipoprotein E-deficient mice.PloS one · 2015Article
- Association of MEF2A gene polymorphisms with coronary artery disease.Iranian Red Crescent medical journal · 2014Article
- Lack of Association between the MEF2A Gene and Coronary Artery Disease in Iranian Families.Iranian journal of basic medical sciences · 2013Article
- Effects of new polymorphisms in the bovine myocyte enhancer factor 2D (MEF2D) gene on the expression rates of the longissimus dorsi muscle.Molecular biology reports · 2012Article
- Promoter variant-dependent mRNA expression of the MEF2A in longissimus dorsi muscle in cattle.DNA and cell biology · 2012Article
- Mutation analysis of the LCE3B/LCE3C genes in Psoriasis.BMC medical genetics · 2010Article
- Molecular genetics of atherosclerosis.Human genetics · 2009Review
- Biomarkers and Bioassays for Cardiovascular Diseases: Present and Future.Biomarker insights · 2008Article
- Myocyte enhancer factor 2 and chorion factor 2 collaborate in activation of the myogenic program in Drosophila.Molecular and cellular biology · 2008Article
- Progress in unraveling the genetics of coronary artery disease and myocardial infarction.Current atherosclerosis reports · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA myocyte enhancer factor 2A (MEF2A) mutation that segregated with coronary artery disease/myocardial infarction (CAD/MI) in a large family has recently been described. Missense mutations in sporadic coronary artery disease patients were also reported. These data suggest that mutations in exons 7 and 11 of MEF2A cause CAD/MI, though the association was refuted by another study.
objectiveTo analyse the genetic variation of exons 7 and 11 in a large cohort of Spanish CAD/MI patients and controls. METHODS AND
resultsA rare polymorphism, P279L, was detected both in patients and controls. Carriers of the 279Leu allele had a threefold risk of suffering CAD/MI compared with controls (p = 0.009; odds ratio = 3.06 (95% confidence interval, 1.17 to 8.06)). In the controls the allele was found only in those under 50 years of age. Exon 11 showed a high degree of heterogeneity caused by a polyglutamine (CAG)n polymorphism, but no significant differences in genotype or allelic frequencies were found.
conclusionsThe 279Leu allele appears to be a genetic risk factor for CAD/MI in the population studied. This effect could be the result of a reduced transcriptional activity on MEF2A with 279Leu.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.