Fatal attractions that trigger inflammation and drive atherosclerotic disease

Abstract

AbstractBackgroundAtherosclerosis is the salient, underlying cause of cardiovascular diseases, such as arrhythmia, coronary artery disease, cardiomyopathy, pulmonary embolism and myocardial infarction. In recent years, atherosclerosis pathophysiology has evolved from a lipid‐based to an inflammation‐centric ideology.MethodsThis narrative review is comprised of review and original articles that were found through the PubMed search engine. The following search terms or amalgamation of terms were used: “cardiovascular disease,” “atherosclerosis,” “inflammation,” “GRP78,” “Hsp60,” “oxidative low‐density lipoproteins,” “aldehyde dehydrogenase,” “β2‐glycoprotein,” “lipoprotein lipase A,” “human cytomegalovirus.” “SARS‐CoV‐2,” “chlamydia pneumonia,” “autophagy,” “thrombosis” and “therapeutics.”ResultsEmerging evidence supports the concept that atherosclerosis is associated with the interaction between cell surface expression of stress response chaperones, including GRP78 and Hsp60, and their respective autoantibodies. Moreover, various other autoantigens and their autoantibodies have displayed a compelling connection with the development of atherosclerosis, including oxidative low‐density lipoproteins, aldehyde dehydrogenase, β2‐glycoprotein and lipoprotein lipase A. Atherosclerosis progression is also concurrent with viral and bacterial activators of various diseases. This narrative review will focus on the contributions of human cytomegalovirus as well as SARS‐CoV‐2 and chlamydia pneumonia in atherosclerosis development. Notably, the interaction of an autoantigen with their respective autoantibodies or the presence of a foreign antigen can enhance inflammation development, which leads to atherosclerotic lesion progression.ConclusionWe will highlight and discuss the complex role of the interaction between autoantigens and autoantibodies, and the presence of foreign antigens in the development of atherosclerotic lesions in relationship to pro‐inflammatory responses.