Abstract
Immune mechanisms play a role in destabilization of atherosclerotic plaque. Vulnerability of the plaque depends on the features of lipid core, stability of the fibrous cap, macrophage and neutrophil infiltration. Also products of leukocytes like metalloproteinases and myeloperoxidase may destabilize the plaque. Destabilized plaque easily ruptures event after minor impact. After plaque rupture, when myocardial infarction happens, immune mechanisms play a role not only in healing, but also may destructively influence left ventricle remodeling. Tumor necrosis factor-α, transforming growth factor-β, toll like receptors and cyclooxygenase are among the most investigated molecules that are thought to influence left ventricular remodeling nowadays. Also autoimmunity (antibodies against contractile proteins) adversely contributes to myocardial remodeling.
Keywords: Atherosclerosis, inflammation, myocardial infarction, autoimmunity, macrophages, cytokines
Related Journals
Related Books
Frontiers in Clinical Drug Research-Dementia
COVID-19: Causes, Transmission, Diagnosis, and Treatment
Skeletal Muscle Health in Metabolic Diseases
AI Innovations in Drug Delivery and Pharmaceutical Sciences; Advancing Therapy through Technology
Anthocyanins: Pharmacology and Nutraceutical Importance
The Roles and Responsibilities of Clinical Pharmacists in Hospital Settings
Common Lip Diseases: A Clinical Guide
Interventional Pain Surgery
Endoscopy and Fetoscopy Techniques for the Brain and Neuroaxis
Bioactive Compounds from Medicinal Plants for Cancer Therapy and Chemoprevention
3