Key result
Transcription factors including GATA2, MEF2A, NF-κB, ATF3, and STAT3 play crucial roles in the pathogenesis of coronary artery disease and myocardial infarction by regulating endothelial function and inflammation.
Transcription factors are critical regulators in the pathogenesis of coronary artery disease and myocardial infarction, representing potential therapeutic targets and biomarkers.
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GWAS variants in CAD/MI may refine risk models; leaves open causal validation and clinical utility.
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-κB) is an important promoter of vascular endothelial growth factor (VEGF)-driven angiogenesis, and its pathway has a key role in atherosclerosis-related complications such as angiogenesis, inflammation, apoptosis, and immune effects. Activating transcription factor 3 (ATF3) may be a novel prognostic biomarker and therapeutic target for atherosclerosis. The important role of signal transducer and activator of transcription 3 (STAT3) (especially in mitochondria) in endothelial cells (EC) dysfunction, inflammation, macrophage polarization and immunity in atherosclerosis.
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Luo et al. (2022) conducted a review in Coronary artery disease and myocardial infarction. Transcription factors (GATA2, MEF2A, NF-κB, ATF3, STAT3) was evaluated. Transcription factors including GATA2, MEF2A, NF-κB, ATF3, and STAT3 play crucial roles in the pathogenesis of coronary artery disease and myocardial infarction by regulating endothelial function and inflammation.
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