Macrophage-Mediated Inflammation in Normal and Diabetic Wound Healing

J Immunol. 2017 Jul 1;199(1):17-24. doi: 10.4049/jimmunol.1700223.

Abstract

The healing of cutaneous wounds is dependent on the progression through distinct, yet overlapping phases of wound healing, including hemostasis, inflammation, proliferation, and resolution/remodeling. The failure of these phases to occur in a timely, progressive fashion promotes pathologic wound healing. The macrophage (MΦ) has been demonstrated to play a critical role in the inflammatory phase of tissue repair, where its dynamic plasticity allows this cell to mediate both tissue-destructive and -reparative functions. The ability to understand and control both the initiation and the resolution of inflammation is critical for treating pathologic wound healing. There are now a host of studies demonstrating that metabolic and epigenetic regulation of gene transcription can influence MΦ plasticity in wounds. In this review, we highlight the molecular and epigenetic factors that influence MΦ polarization in both physiologic and pathologic wound healing, with particular attention to diabetic wounds.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Differentiation
  • Diabetes Complications / immunology
  • Diabetes Mellitus / immunology*
  • Epigenesis, Genetic
  • Gene Expression Regulation
  • Humans
  • Inflammation / immunology*
  • Inflammation Mediators / immunology
  • Macrophages / immunology*
  • Mice
  • Wound Healing / immunology*

Substances

  • Inflammation Mediators