Association Between Genetic Variants and Circulating Biomarkers of Extracellular Matrix Remodelling in Indian Patients With Acute and Recurrent Myocardial Infarction
1
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Objective: Conventional risk factors only partially explain the rising incidence of myocardial infarction (MI). The effect of genetic polymorphisms of extracellular matrix (ECM) remodelling markers on atherosclerotic process and thereby, major adverse cardiovascular events (MACE) have not been much studied. This research examines the relationships of single nucleotide polymorphisms (SNPs) of matrix metalloproteinases (MMPs) such as MMP-9 (−1562 C/T and R279Q), MMP-3 (−1612 5A/6A), and the tissue inhibitors of metalloproteinases (TIMP) namely TIMP-1 (−372 T/C) in patients of acute (AMI) and recurrent myocardial infarction (RMI). Methods: This study, conducted in an Indian population, included 200 consecutively enrolled patients presenting within 24 hours of MI, confirmed by clinical and diagnostic criteria, with exclusions for major comorbidities, and categorized into first-time AMI and RMI cases. SNPs were identified by polymerase chain reaction-restriction fragment length polymorphism. Serum MMP-9, MMP-3 and TIMP-1 were measured using enzyme-linked immunosorbent assay. Statistical analysis was performed with significance level set at p<0.05. Results: Significantly high levels of serum MMP-9 (62.87 vs. 60.76 vs. 60.77 pg/mL; p=0.045) was seen in AG phenotype of MMP-9 R279Q polymorphism compared to AA and GG phenotypes. AMI and RMI patients showed no significant difference in the distribution of SNP genotypes of MMP-9 R279Q (χ2=2.220, p=0.330), MMP-9 (−1562 C/T) (χ2=3.298, p=0.192), MMP-3 (−1612 5A/6A) (χ2=1.215, p=0.545) and TIMP-1 (−372 T/C) (χ2=0.005, p=0.997). Conclusion: Genetic polymorphisms play a crucial role in regulating ECM marker levels and novel biomarkers, such as MMP-3, MMP-9, and TIMP-1, may be linked to MI susceptibility. Further research on therapeutic approaches targeting ECM remodelling could potentially improve MACE incidence.
Abstract
Objective: Conventional risk factors only partially explain the rising incidence of myocardial infarction (MI). The effect of genetic polymorphisms of extracellular matrix (ECM) remodelling markers on atherosclerotic process and thereby, major adverse cardiovascular events (MACE) have not been much studied. This research examines the relationships of single nucleotide polymorphisms (SNPs) of matrix metalloproteinases (MMPs) such as MMP-9 (−1562 C/T and R279Q), MMP-3 (−1612 5A/6A), and the tissue inhibitors of metalloproteinases (TIMP) namely TIMP-1 (−372 T/C) in patients of acute (AMI) and recurrent myocardial infarction (RMI). Methods: This study, conducted in an Indian population, included 200 consecutively enrolled patients presenting within 24 hours of MI, confirmed by clinical and diagnostic criteria, with exclusions for major comorbidities, and categorized into first-time AMI and RMI cases. SNPs were identified by polymerase chain reaction-restriction fragment length polymorphism. Serum MMP-9, MMP-3 and TIMP-1 were measured using enzyme-linked immunosorbent assay. Statistical analysis was performed with significance level set at p<0.05. Results: Significantly high levels of serum MMP-9 (62.87 vs. 60.76 vs. 60.77 pg/mL; p=0.045) was seen in AG phenotype of MMP-9 R279Q polymorphism compared to AA and GG phenotypes. AMI and RMI patients showed no significant difference in the distribution of SNP genotypes of MMP-9 R279Q (χ2=2.220, p=0.330), MMP-9 (−1562 C/T) (χ2=3.298, p=0.192), MMP-3 (−1612 5A/6A) (χ2=1.215, p=0.545) and TIMP-1 (−372 T/C) (χ2=0.005, p=0.997). Conclusion: Genetic polymorphisms play a crucial role in regulating ECM marker levels and novel biomarkers, such as MMP-3, MMP-9, and TIMP-1, may be linked to MI susceptibility. Further research on therapeutic approaches targeting ECM remodelling could potentially improve MACE incidence.