1 Relationship between immunometabolic stress and atherosclerosis
The underlying cause of heart attacks and strokes is atherosclerosis(Jones et al., 2021). High LDL cholesterol levels and apolipoprotein B (apoB) 100, the primary structural protein of LDL, are directly connected with the risk of atherosclerotic cardiovascular events, according to studies (ASCVE)(Tokgozoglu and Kayikcioglu, 2021). Infiltration and retention of apoB-containing lipoproteins in artery walls are critical beginning events that initiate an inflammatory response and promote atherosclerosis progression(Banaszak and Ranatunga, 2008). Endothelial dysfunction is caused by arterial damage, which promotes the alteration of apoB-containing lipoproteins and monocyte infiltration into the subendothelial region. Internalization of apoB-containing lipoproteins by macrophages increases the development of foam cells, a defining characteristic of the fatty streak phase of atherosclerosis(Laccotripe et al., 1997). Inflammation of macrophages increases oxidative stress and cytokine/chemokine release, leading to an increase in LDL/residual oxidation, endothelial cell activation, monocyte recruitment, and foam cell formation. All lipoproteins containing apoB are atherogenic, and residual lipoproteins high in triglycerides and Lp(a) cause atherothrombosis(Enas et al., 2019).