†These authors contributed equally.
Academic Editor: Ioanna-Katerina Aggeli
Coronary artery disease (CAD) and its main complication, myocardial infarction
(MI), is a complex disease caused by environmental and genetic factors and their
interaction. Family-based linkage analysis and genome-wide association studies
have indicated many of genetic variations related to CAD and MI in recent years.
Some are in the coding sequence, which mediates the coding protein, while others
are in the non-coding region, which affects the expression of adjacent genes and
forms differential gene expression. These variants and differential expressions
will have varying degrees of impact on the development of the cardiovascular
system and normal heart electrical activity function, subsequently leading to CAD
and MI. Among these affected genes, some Transcription Factors (TFs), as
important means of transcriptional regulation, have a key role in the
pathogenesis of coronary artery disease and myocardial infarction. The GATAs
binding protein 2 (GATA2) enhances monocyte adhesion and promoted vessel wall
permeabilization through vascular EC adhesion molecule 1 (VCAM-1) upregulation,
further revealing its atherosclerosis-promoting role. Myocyte enhancer factor 2
(MEF2) has a role in fostering many functions of the atherosclerotic endothelium
and is a potential therapeutic target for atherosclerosis, thrombosis, and
inflammation. Nuclear factor-kappa B (NF-