Identification of Risk Genes Associated with Myocardial Infarction-Big Data Analysis and Literature Review

Int J Mol Sci. 2022 Nov 30;23(23):15008. doi: 10.3390/ijms232315008.

Abstract

Acute myocardial infarction occurs when blood supply to a particular coronary artery is cut off, causing ischemia or hypoxia and subsequent heart muscle destruction in the vascularized area. With a mortality rate of 17% per year, myocardial infarction (MI) is still one of the top causes of death globally. Numerous studies have been done to identify the genetic risk factors for myocardial infarction, as a positive family history of heart disease is one of the most potent cardiovascular risk factors. The goal of this review is to compile all the information currently accessible in the literature on the genes associated with AMI. We performed a big data analysis of genes associated with acute myocardial infarction, using the following keywords: "myocardial infarction", "genes", "involvement", "association", and "risk". The analysis was done using PubMed, Scopus, and Web of Science. Data from the title, abstract, and keywords were exported as text files and imported into an Excel spreadsheet. Its analysis was carried out using the VOSviewer v. 1.6.18 software. Our analysis found 28 genes which are mostly likely associated with an increased risk for AMI, including: PAI-1, CX37, IL18, and others. Also, a correlation was made between the results obtained in the big data analysis and the results of the review. The most important genes increasing the risk for AMI are lymphotoxin-a gene (LTA), LGALS2, LDLR, and APOA5. A deeper understanding of the underlying functional genomic circuits may present new opportunities for research in the future.

Keywords: association; gene; myocardial infarction; risk.

Publication types

  • Review

MeSH terms

  • Data Analysis
  • Galectin 2 / genetics
  • Humans
  • Lymphotoxin-alpha
  • Myocardial Infarction*
  • Risk Factors

Substances

  • Lymphotoxin-alpha
  • Galectin 2

Grants and funding

This research received no external funding.