Relationship of matrix metalloproteinase-3 -11715A/6A polymorphism (rs35068180) and dilated cardiomyopathy
Open Access
- 18 November 2020
- journal article
- Published by Silicea - Poligraf, LLC in Russian Journal of Cardiology
- Vol. 25 (10), 3960
- https://doi.org/10.15829/1560-4071-2020-3960
Abstract
Aim. To study the relationship of matrix metalloproteinase-3 (MMP3) genetic polymorphism and dilated ischemic cardiomyopathy (DCM), as well as idiopathic cardiomyopathy (ICM) of unknown etiology.Material and methods. A total of 221 patients with DCM and ICM were examined (mean age, 55,30±9,69 years). The group of ischemic DCM consisted of 111 people (99 men (89,2%) and 12 women (10,8%)). The mean age of DCM subjects was 51,73±9,74 years (male subgroup, 51,00±8,96 years; female subgroup, 57,75±3,71 years). The ICM group consisted of 110 people (100 men (91,5%) and 10 women (8.5%)). The mean age of ICM subjects was 58,68±8.38 years (male subgroup, 58,29±8.,6 years; female subgroup, 62,90±6,29 years). The control group of subjects (n=121) consisted of healthy people without cardiovascular diseases (mean age, 53,6±4,8 years). All patients of the experimental group underwent routine diagnostic tests, as well as coronary angiography. In case of suspected myocarditis, cardiac magnetic resonance imaging was performed. All patients underwent polymerase chain reaction to determine the MMP3-11715A/6A polymorphism (rs35068180).Results. In patients with cardiomyopathy, regardless of the disease origin, significant differences were verified in comparison with the control group. Allele 6A (65,8% vs 59,3%, p=0,044) and genotype 6A/6A (42,1% vs 32,6%, p=0,099) were found significantly more frequently in patients with cardiomyopathy than in the control group. In addition, despite various etiological factors, the pathogenetic involvement of MMP3 is likely to have a general direction.Conclusion. In all patients with cardiomyopathy, the prevalence of MMP3 gene A allele was shown. Due to decrease in the transcription activity in homozygous 6A allele, the stromelysin level in arterial walls also decreases. This promotes the activation of procollagenase-1, the deposition of extracellular matrix and cardiac remodelingKeywords
This publication has 14 references indexed in Scilit:
- Variations in matrix metalloproteinase-1, -3, and -9 genes and the risk of acute coronary syndrome and coronary artery disease in the Chinese Han populationCoronary Artery Disease, 2013
- Matrix metalloproteinase-1, -3, and -9 gene polymorphisms and the risk of idiopathic dilated cardiomyopathy in a Chinese Han populationClinical Biochemistry, 2007
- Classification of the cardiomyopathies: a position statement from the european society of cardiology working group on myocardial and pericardial diseasesEuropean Heart Journal, 2007
- Influence of matrix metalloproteinase genotype on cardiovascular disease susceptibility and outcomeCardiovascular Research, 2006
- Matrix Metalloproteinase-3 Genotype Contributes to Age-Related Aortic Stiffening Through Modulation of Gene and Protein ExpressionCirculation Research, 2003
- Interaction between smoking and the stromelysin‐1 (MMP3) gene 5A/6A promoter polymorphism and risk of coronary heart disease in healthy menAnnals of Human Genetics, 2002
- Induction of oxidative stress and disintegrin metalloproteinase in human heart end-stage failureAmerican Journal of Physiology-Lung Cellular and Molecular Physiology, 2002
- Matrix Metalloproteinases: From Biology to Therapeutic Strategies in Cardiovascular DiseaseJournal of Investigative Medicine, 2001
- Matrix Metalloproteinase Inhibition After Myocardial InfarctionCirculation Research, 2001
- The Clinical Course of Idiopathic Dilated CardiomyopathyAnnals of Internal Medicine, 1992