Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction

Cell Mol Biol Lett. 2023 Oct 19;28(1):81. doi: 10.1186/s11658-023-00491-4.

Abstract

Early and prompt reperfusion therapy has markedly improved the survival rates among patients enduring myocardial infarction (MI). Nonetheless, the resulting adverse remodeling and the subsequent onset of heart failure remain formidable clinical management challenges and represent a primary cause of disability in MI patients worldwide. Macrophages play a crucial role in immune system regulation and wield a profound influence over the inflammatory repair process following MI, thereby dictating the degree of myocardial injury and the subsequent pathological remodeling. Despite numerous previous biological studies that established the classical polarization model for macrophages, classifying them as either M1 pro-inflammatory or M2 pro-reparative macrophages, this simplistic categorization falls short of meeting the precision medicine standards, hindering the translational advancement of clinical research. Recently, advances in single-cell sequencing technology have facilitated a more profound exploration of macrophage heterogeneity and plasticity, opening avenues for the development of targeted interventions to address macrophage-related factors in the aftermath of MI. In this review, we provide a summary of macrophage origins, tissue distribution, classification, and surface markers. Furthermore, we delve into the multifaceted roles of macrophages in maintaining cardiac homeostasis and regulating inflammation during the post-MI period.

Keywords: Hemostasis; Inflammation; Macrophage; Myocardial infarction; Polarization.

Publication types

  • Review

MeSH terms

  • Animals
  • Heart Failure*
  • Humans
  • Inflammation / pathology
  • Macrophages
  • Mice
  • Mice, Inbred C57BL
  • Myocardial Infarction* / pathology
  • Myocardium / pathology