Novel strategies for targeting neutrophil against myocardial infarction

Abstract

Inflammation is a crucial factor in cardiac remodeling after acute myocardial infarction (MI). Neutrophils, as the first wave of leukocytes to infiltrate the injured myocardium, exacerbate inflammation and cardiac injury. However, therapies that deplete neutrophils to manage cardiac remodeling after MI have not consistently produced promising outcomes. Recent studies have revealed that neutrophils at different time points and locations may have distinct functions. Thus, transferring neutrophil phenotypes, rather than simply blocking their activities, potentially meet the needs of cardiac repair. In this review, we focus on discussing the fate, heterogeneity, functions of neutrophils, and attempt to provide a more comprehensive understanding of their roles and targeting strategies in MI. We highlight the strategies and translational potential of targeting neutrophils to limit cardiac injury to reduce morbidity and mortality from MI.

Keywords: Colchicine (PubChem CID: 6167); Disulfiram (PubChem CID: 3117); Fate transition; Function; Heterogeneity; Methotrexate (PubChem CID: 126941); Myocardial infarction; Necrosulfonamide (PubChem CID: 1566236); Neutrophils; Salvianolic acid E (PubChem CID: 86278266).