High-glucose environment disturbs the physiologic functions of keratinocytes: Focusing on diabetic wound healing

J Dermatol Sci. 2016 Nov;84(2):121-127. doi: 10.1016/j.jdermsci.2016.07.008. Epub 2016 Jul 16.

Abstract

Impaired wound healing is a common and potentially serious complication in patients with diabetes. In recent years, disturbed physiologic functions of epidermal keratinocytes have been found to play a central role in the poor healing ability of diabetic wounds. Factors involving keratinocytes that may contribute to the dysfunctional wound healing process in diabetes include impaired keratinocyte migration and proliferation, gap junction abnormalities, chronic inflammation, chronic infections associated with defective innate immunity, impaired angiogenesis, increased oxidative stress, and abnormal expression of matrix metalloproteinases (MMPs). In this review article, we provide evidence from the scientific literature for the molecular mechanisms of delayed wound healing in diabetes, with particular emphasis on keratinocytes. Elucidating the spectrum of molecular and functional abnormalities in keratinocytes induced by high-glucose environment may lead to more effective and individualized therapeutic strategies for the prevention and management of chronic diabetic wounds.

Keywords: Diabetes; High-glucose environment; Keratinocytes; Wound healing.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Movement
  • Cell Proliferation
  • Diabetes Mellitus / drug therapy*
  • Diabetes Mellitus / metabolism
  • Epidermis / metabolism
  • Gap Junctions / metabolism
  • Glucose / chemistry*
  • Hemostasis
  • Humans
  • Immunity, Innate
  • Inflammation
  • Keratinocytes / cytology*
  • Keratinocytes / drug effects
  • Matrix Metalloproteinases / metabolism
  • Mice
  • Oxidative Stress
  • Wound Healing / physiology*

Substances

  • Matrix Metalloproteinases
  • Glucose