Fatal attractions that trigger inflammation and drive atherosclerotic disease

Abstract

BackgroundAtherosclerosis 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.

Crosstalk between Inflammation and Atherosclerosis in Rheumatoid Arthritis and Systemic Lupus Erythematosus: Is There a Common Basis?

“…In addition, emerging evidence points to a role of viral and bacterial triggers in the pathogenesis of atherosclerosis [ 39 ], triggers that are also implicated in the pathogenesis of autoimmune diseases [ 40 ], hepatitis viruses, periodontal bacteria, LPS, etc., due to molecular mimicry phenomena. Further research has revealed the presence of autoantibodies that can enhance the inflammatory process, such as antibodies against glucose-regulated protein 78 (GRP78) and those against heat shock proteins 60 and 90 (HSP60, HSP90) [ 39 ].…”

Myocardial Expression of Pluripotency, Longevity, and Proinflammatory Genes in the Context of Hypercholesterolemia and Statin Treatment

“…In the past two decades, a robust body of literature has linked vascular inflammation to atheromatosis [1]. Toll-like receptors (TLRs) have been identified as primary contributors to the inflammatory processes that fuel the progression of atherosclerosis [2,3].…”

“…Alongside established biomarkers, recent studies are investigating novel atheroprotective agents such as klotho (an anti-aging hormone) and stem cell-related genes including HOXA5 and Krüppel-like factors (KLF). Additional attention is directed towards proatherogenic pluripotency factors such as NANOG and HIF1α [1,[6][7][8]. Dysregulation of their expression has been implicated in various aspects of atherogenesis, including increased release of pro-inflammatory cytokines and chemokines, upregulation of adhesion molecules, migration and phenotypic switching of vascular smooth muscle cells (VSMCs), alterations in extracellular matrix, oxidative stress, and the development of neointimal hyperplasia [6,9,10].…”