Macrophages after myocardial infarction: Mechanisms for repairing and potential as therapeutic approaches

Int Immunopharmacol. 2024 Dec 25;143(Pt 3):113562. doi: 10.1016/j.intimp.2024.113562. Epub 2024 Nov 12.

Abstract

Macrophages - one of the crucial immune cells, are recruited to the cardiac tissue by chemokines, cytokines and upregulated endothelial adhesion molecules after myocardial infarction (MI). During the course of inflammation in the cardiac tissue, necrotic cells and matrix debris is phagocytosed by M1 macrophages. During the resolution phase of cardiac inflammation, M2 macrophages promote cardiac recovery. Suppression or over expression of both the M1 and M2 macrophage subtypes significantly affect the reparation of infarction. Stem cells therapy, cytokine regulation and immune cells therapy are considered as effective interventions to regulate the phenotypic transformation of cardiac macrophages after MI. Intervention with macrophages in the myocardium has shown unique advantages. In this review, the mechanisms and role of macrophages in the development of MI are elaborated in detail, the promising therapeutic methods for regulating macrophage phenotypes, their limitations and possible future research directions are discussed.

Keywords: Cardiac repair; Macrophages; Myocardial infarction; Polarization; Therapeutic strategies.

Publication types

  • Review

MeSH terms

  • Animals
  • Cytokines / immunology
  • Cytokines / metabolism
  • Humans
  • Macrophages* / immunology
  • Myocardial Infarction* / immunology
  • Myocardial Infarction* / therapy
  • Myocardium / immunology
  • Myocardium / metabolism
  • Myocardium / pathology
  • Stem Cell Transplantation

Substances

  • Cytokines