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Inflammation and Immunological Responses in Atherosclerosis: Origins and Therapeutic Targets for Innovative Cardiovascular Disease (CVD) Therapies

Glory Coppe

This study focuses on atherosclerosis, a prominent cause of cardiovascular disease (CVD). Atherosclerosis is a chronic inflammatory disorder characterised by immunological competent cells in lesions that primarily generate proinflammatory cytokines. The presence of dead cells and oxidised versions of low density lipoproteins (oxLDL) is significant in this syndrome. The rupture of atherosclerotic plaques is the main cause of CVD. At larger concentrations, oxLDL has features that promote inflammation and immunological activation, causing cell death. It also includes inflammatory phospholipids, notably phosphorylcholine (PC), which is an intriguing epitope. Antibodies that target PC (anti-PC) may have atheroprotective benefits, possibly due to their anti-inflammatory qualities. While the participation of bacteria and viruses in atherosclerosis has been discussed, direct proof has been difficult to come by, and antibiotic studies have failed. Heat shock proteins have the potential to be targets for atherogenic immune responses. Pro-inflammatory cytokines, chemokines, and lipid mediators are other contributors in plaque rupture. To establish inflammation as a cause of atherosclerosis and CVD, clinical trials using anti-inflammatory and immune-modulatory therapy are required. This review investigates the possible origins of immunological responses and inflammation in atherosclerosis, as well as therapeutic techniques that target inflammation for innovative CVD therapies.