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).