Open Access

REVIEW

Biochemical association between the prevalence of genetic polymorphism and myocardial infarction

MOMINA SHAHID¹, KANWAL REHMAN², MUHAMMAD SAJID HAMID AKASH^1,*, SHALEEM SUHAIL¹, SUMBAL RASHEED¹, MUHAMMAD IMRAN^3,4, MOHAMMED A. ASSIRI^3,4

1 Department of Pharmaceutical Chemistry, Government College University, Faisalabad, 38000, Pakistan
2 Department of Pharmacy, The Women University, Multan, 60000, Pakistan
3 Research Center for Advanced Materials Science (RCAMS), King Khalid University, Abha, 62413, Saudi Arabia
4 Department of Chemistry, Faculty of Science, King Khalid University, Abha, 62413, Saudi Arabia

* Corresponding Author: MUHAMMAD SAJID HAMID AKASH. Email:

(This article belongs to the Special Issue: )

BIOCELL 2023, 47(3), 473-484. https://doi.org/10.32604/biocell.2023.025930

Received 05 August 2022; Accepted 24 October 2022; Issue published 03 January 2023

Abstract

Genetic polymorphism has a vital role in the pathogenesis and development of myocardial infarction (MI). Single nucleotide polymorphism at any one of the amino acid sequences can result in a diseased state. A single gene can exhibit genetic polymorphism at more than one position giving rise to different variants. Genetic polymorphism of angiotensinogen (AGT) M235T, AGT T174M, and angiotensin-1-converting enzyme (ACE) I/D, endothelial nitric oxide synthase (eNOS), and methylenetetrahydrofolate reductase (MTHFR) can be a risk factor for MI. However, it is important to study the prevalence of genetic polymorphisms of these genes among different populations. MI is influenced by genetic polymorphism of various genes, including AGT, ACE, eNOS, MTHFR, etc. However, the association of genetic polymorphism of these genes varies among different populations, but different ethnic groups could show contradictory results. These genes have shown a positive association with risks of MI in some populations, whereas the results have not been consistent with every ethnic group. In this article, we have summarized the genetic variations in the aforementioned genes and their association with MI.

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Keywords

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