Contributions of Macrophages in the Disease Pathology of Myocardial Infarction and Atherosclerosis: A Literature Review

Abstract

Introduction: Macrophages have been shown to play a role in the disease pathology of myocardial infarction and atherosclerosis, two prominent cardiovascular diseases. Understanding the mechanisms by which macrophages contribute to disease onset can serve as a valuable resource for the development of new therapeutics. This study specifically aims to identify the roles macrophages play in the regulation and progression of myocardial infarction and atherosclerosis in human and mice models, while highlighting current and developing treatments that target macrophages to prevent or delay these diseases.

Methods: This review examines studies and previous reviews in the last 20 years that report proinflammatory mediators secreted by pro-inflammatory (M1-like) macrophages in humans and mice that are affected by myocardial infarction or atherosclerosis or have undergone simulated conditions.

Discussion: Pro-inflammatory M1 macrophages influence both myocardial infarction and atherosclerosis via the secretion of proinflammatory mediators IL-1β, IL-1∝, IL-6, TNF-∝, VCAM-1, MMP-9, and MCP-1. These mediators are shown to promote adverse cardiac remodelling events in individuals with myocardial infarction including inflammation, increase in the infarcted area, and worsened left ventricular systolic function. For those with atherosclerosis, mediator release is correlated with lesion and plaque development due to increased leukocyte and lymphocyte migration. Mediators that directly influence either disease are also reported. As atherosclerosis is a risk factor for myocardial infarction, the overall promotion of atherosclerosis by both shared and specific inflammatory mediators therefore increases the likelihood an individual undergoes myocardial infarction. Current and developing treatments for myocardial infarction revolve around inhibiting mediator release and activity, whereas inducing macrophage polarization, inhibiting scavenger receptor activity, and inducing autophagy are the focus of therapeutic intervention for atherosclerosis.

Conclusion: Proinflammatory macrophages show a prominent role in the pathogenesis of myocardial infarction and atherosclerosis, including the body’s ability to recover from these diseases. Further research should involve identifying macrophage phenotypes and improvements in drug delivery methods may serve as future avenues in improvement for macrophage-based medicines of common CVDs.