Methylation status and levels of tumor necrosis factor receptor superfamily member 4 (TNFRSF4) in myocardial infarction

The most common form of Coronary heart disease (CHD) is Myocardial Infarction (MI). It is responsible for over 15% of mortality each year, majority of people suffering from non-ST-segment elevation myocardial infarction (NSTEMI) than ST-segment elevation myocardial infarction (STEMI).According to World health organization (WHO), it is estimated that 7.5 million deaths were due to CHD in 2015.

MI is caused by decreased or complete cessation of blood flow to a portion of the myocardium. Patients can present with chest discomfort or pressure that can radiate to the neck, jaw, shoulder, or arm. MI may be associated with electrocardiogram (ECG)changes and elevated biochemical markers such as cardiac troponins.

The TNFSF4 (tumor necrosis factor ligand superfamily member 4) gene is expressed by activated B cells, endothelial cells, and activated CD4+ and CD8+ T-cells. The TNFRSF Rc, TNFRSF4 (tumor necrosis factor receptor superfamily member 4) is also expressed on activated T cells. When gets activated, T cells produce proinflammatory cytokines, which are largely responsible for plaque rupture and thrombus formation. The TNFSF4/TNFRSF4 pathway plays a role in atherosclerosis and atherosclerotic disease.

DNA methylation is an epigenetic mechanism consisting in which chemical modifications of cytosines, mostly followed by guanines (CpGs). Epigenome-wide association studies (EWASs) make it possible to find DNA methylation biomarkers of different traits and outcomes.