Susceptibility of MMP3 gene polymorphism to coronary artery disease: A meta-analysis

Liu Wenwang1

  • 1Beijing Hospital of Integrated Chinese & Western Medicine, Department of Clinical Laboratory, Beijing China.

PubMed
Abstract

Insights

This meta-analysis investigates the link between the MMP3-1612 5A/6A polymorphism and coronary artery disease (CAD) risk. It synthesizes data from 18 studies to clarify controversial findings on their association.

Area of Science:

  • Genetics and Cardiovascular Disease Research
  • Molecular Biology and Disease Mechanisms

Background:

  • The association between the MMP3-1612 5A/6A polymorphism and coronary artery disease (CAD) risk remains debated.
  • Existing research presents conflicting conclusions regarding this genetic susceptibility.

Purpose of the Study:

  • To conduct a comprehensive meta-analysis to establish the precise relationship between the MMP3-1612 5A/6A polymorphism and the risk of developing CAD.
  • To resolve controversies surrounding the genetic predisposition to CAD conferred by this specific matrix metalloproteinase 3 (MMP3) variant.

Main Methods:

  • A systematic literature search was performed across major databases (PubMed, Web of Science, Cochrane Library, CNKI, VIP, Wanfang) for studies published before July 2019.
  • Data from 18 eligible studies examining the MMP3-1612 5A/6A polymorphism and CAD were extracted independently by two researchers.
  • Statistical analysis, including odds ratio (OR) and 95% confidence interval (CI) calculation, was performed using RevMan 5.3 and STATA 12.0.

Main Results:

  • The meta-analysis synthesized data from 18 relevant studies.
  • Odds ratios and 95% confidence intervals were calculated to quantify the association.
  • Disagreements in data extraction were resolved by a third researcher to ensure accuracy.

Conclusions:

  • The meta-analysis provides a synthesized view on the controversial link between MMP3-1612 5A/6A and CAD risk.
  • The study aims to offer a more definitive conclusion on the genetic susceptibility conferred by this polymorphism.
  • Further research may be warranted to fully elucidate the role of MMP3-1612 5A/6A in CAD pathogenesis.