ArticlePloS one2011
Association of 25 bp deletion in MYBPC3 gene with left ventricle dysfunction in coronary artery disease patients.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Identification of Two Homozygous Variants inGenes · 2023Article
- South Asian-SpecificFrontiers in cardiovascular medicine · 2021Article
- Genetic, clinical, molecular, and pathogenic aspects of the South Asian-specific polymorphic MYBPC3Biophysical reviews · 2020Review
- Reevaluation of the South AsianCirculation. Genomic and precision medicine · 2020Article
- South Asian-SpecificCirculation. Genomic and precision medicine · 2020Article
- Sarcomeric Gene Variants and Their Role with Left Ventricular Dysfunction in Background of Coronary Artery Disease.Biomolecules · 2020Review
- Altered C10 domain in cardiac myosin binding protein-C results in hypertrophic cardiomyopathy.Cardiovascular research · 2019Article
- Defining genotype-phenotype relationships in patients with hypertrophic cardiomyopathy using cardiovascular magnetic resonance imaging.PloS one · 2019Article
- Association of Cardiomyopathy With MYBPC3 D389V and MYBPC3Δ25bpIntronic Deletion in South Asian Descendants.JAMA cardiology · 2018Article
- Clinical Application of Genetic Testing in Heart Failure.Current heart failure reports · 2017Review
- High-Throughput Diagnostic Assay for a Highly Prevalent Cardiomyopathy-AssociatedJournal of molecular biomarkers & diagnosis · 2016Article
- Role of common sarcomeric gene polymorphisms in genetic susceptibility to left ventricular dysfunction.Journal of genetics · 2016Article
- Recent Advances in the Molecular Genetics of Familial Hypertrophic Cardiomyopathy in South Asian Descendants.Frontiers in physiology · 2016Review
- The genetic landscape of cardiomyopathy and its role in heart failure.Cell metabolism · 2015Review
- CXCL12-CXCR4 axis promotes the natural selection of breast cancer cell metastasis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- MYBPC3's alternate ending: consequences and therapeutic implications of a highly prevalent 25 bp deletion mutation.Pflugers Archiv : European journal of physiology · 2014Review
- Role of angiotensin II type I (AT1 A1166C) receptor polymorphism in susceptibility of left ventricular dysfunction.Indian heart journalArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleMutations in MYBPC3 encoding cardiac myosin binding protein C are common genetic cause of hereditary cardiac myopathies. An intronic 25-bp deletion in MYBPC3 at 3' region is associated with dilated (DCM) and hypertrophic (HCM) cardiomyopathies in Southeast Asia. However, the frequency of MYBPC3 25 bp deletion and associated clinical presentation has not been established in an unrelated cohort of left ventricular dysfunction (LVD) secondary to coronary artery disease (CAD) patients.
objectiveWe sought to determine the role of MYBPC3 25 bp polymorphism on LVD in two cohorts of CAD patients. METHODS AND
resultsThe study included 265 consecutive patients with angiographically confirmed CAD and 220 controls. MYBPC3 25 bp polymorphism was determined by polymerase chain reaction. Our results showed that carrier status of MYBPC3 25 bp deletion was associated with significant compromised left ventricle ejection fraction (LVEF ≤45) in CAD patients (p value = <0.001; OR = 4.49). To validate our results, we performed a replication study in additional 140 cases with similar clinical characteristics and results again confirmed consistent findings (p = 0.029; OR = 3.3). Also, presence of the gene deletion did not have significant association in CAD patients with preserved ejection fraction (LVEF>45) (p value = 0.1; OR = 2.3).
conclusionThe frequency of MYBPC3 DW genotype and D allele was associated with compromised LVEF implying that genetic variants of MYBPC3 encoding mutant structural sarcomere protein could increase susceptibility to left ventricular dysfunction. Therefore, 25 bp deletion in MYBPC3 may represent a genetic marker for cardiac failure in CAD patients from Southeast Asia.
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