The role of inflammatory response in the development of atherosclerosis, myocardial infarction, and remodeling

Abstract

Inflammation is an intrinsic part of the body’s immune response, significantly influencing a myriad of physiological and pathological processes. There is now clinical and experimental evidence suggesting that inflammation accelerates atherosclerosis and its associated complications. The presence of macrophages, T and B cells inside the atherosclerotic plaque fueled this concept and steered subsequent research endeavors toward understanding the pathophysiology of atherosclerosis including plaque formation and destabilization leading to plaque rupture resulting in myocardial injury and remodeling. Understanding the mechanism behind atherosclerosis will aid in developing appropriate treatment interventions. Shifting research and drug development from a singular focus on cholesterol-lowering agents to include adjunctive anti-inflammatory therapies is crucial. Targeting a root cause, i.e., inflammation, will help decrease the incidence and progression of atherosclerosis and improve patient outcomes. In this review, we aim to discuss the current understanding of the intricate role of inflammation in the pathogenesis of atherosclerosis, myocardial infarction, and cardiac remodeling. This synthesis will encompass an exploration of the various inflammatory cells involved, the intricate network of chemokines orchestrating inflammatory responses, and the pathways that underpin these cardiovascular conditions. Furthermore, we will explore promising diagnostic and therapeutic strategies aimed at addressing inflammation in cardiovascular diseases. These include interventions such as colchicine, monoclonal antibodies, and nanoparticles designed to deliver and accumulate drugs at the molecular level within cells.

Keywords

Atherosclerosis / myocardial infarction / inflammation / cardiac remodeling / atheroma / nanoparticles

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