Related Experiment Video
Updated: Jul 4, 2025
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Fatal attractions that trigger inflammation and drive atherosclerotic disease
Hitesh Sharma1, Karen Mossman2, Richard C Austin1
1Division of Nephrology, Department of Medicine, McMaster University, The Research Institute of St. Joe's Hamilton and the Hamilton Centre for Kidney Research, Hamilton, Ontario, Canada.
Insights
Atherosclerosis development is linked to inflammation, autoantibodies, and foreign antigens like viruses and bacteria. Understanding these interactions is key to managing cardiovascular disease progression.
Area of Science:
- Cardiovascular Science
- Immunology
- Pathophysiology
Background:
- Atherosclerosis is a primary cause of cardiovascular diseases.
- Pathophysiology has shifted from a lipid-centric to an inflammation-centric view.
- Key cardiovascular diseases include arrhythmia, coronary artery disease, and myocardial infarction.
Purpose of the Study:
- To review the role of inflammation in atherosclerosis.
- To explore the connection between autoantigens, autoantibodies, and atherosclerosis.
- To examine the impact of foreign antigens on atherosclerotic lesion development.
Main Methods:
- Narrative review of PubMed-sourced articles.
- Search terms included "atherosclerosis," "inflammation," "autoantibodies," and specific pathogens.
- Focused on stress response chaperones, autoantigens, and infectious agents.
Main Results:
- Stress response chaperones (GRP78, Hsp60) and autoantibodies are linked to atherosclerosis.
- Other autoantigens (oxidative LDL, aldehyde dehydrogenase) also correlate with disease.
- Viral (HCMV, SARS-CoV-2) and bacterial (Chlamydia pneumoniae) infections contribute to atherosclerosis progression.
Conclusions:
- Autoantigen-autoantibody interactions promote inflammation in atherosclerosis.
- Foreign antigens can enhance inflammation, driving atherosclerotic lesion progression.
- Understanding these complex interactions is crucial for therapeutic strategies.
Background:
Atherosclerosis 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.
Methods:
This 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."
Results:
Emerging 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.
Conclusion:
We 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.
Related Concept Videos
01:38Inflammation
01:17Ischemic Heart Disease: Overview
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...
01:31Lipid-derived Compounds in the Human Body
Fat-soluble Vitamins
Fat-soluble vitamins, including vitamins A, D, E, and K, are required in minimal quantities, but their deficiencies can lead to severely abnormal physiological conditions. For example, vitamin A deficiency can cause night blindness, dry skin,...
01:24Chronic Pancreatitis I: Introduction
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
01:30Inflammatory Response I: Vascular and Cellular
01:28Inflammatory Response
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...