GSK3 modulation in acute lung injury, myocarditis and polycystic kidney disease-related aneurysm

Biochim Biophys Acta Mol Cell Res. 2020 Nov;1867(11):118798. doi: 10.1016/j.bbamcr.2020.118798. Epub 2020 Jul 18.

Abstract

GSK3 are involved in different physical and pathological conditions and inflammatory regulated by macrophages contribute to significant mechanism. Infection stimuli may modulate GSK3 activity and influence host cell adaption, immune cells infiltration or cytokine expressions. To further address the role of GSK3 modulation in macrophages, the signal transduction of three major organs challenged by endotoxin, virus and genetic inherited factors are briefly introduced (lung injury, myocarditis and autosomal dominant polycystic kidney disease). As a result of pro-inflammatory and anti-inflammatory functions of GSK3 in different microenvironments and stages of macrophages (M1/M2), the rational resolution should be considered by adequately GSK3.

Keywords: HMGB1/IL-17A/autophagy; M1/M2 macrophages; Mitotic catastrophe; PI3K/Akt/GSK3β/MCP-1 axis; Podocyte; Pulmonary edema.

Publication types

  • Review

MeSH terms

  • Acute Lung Injury / genetics*
  • Acute Lung Injury / pathology
  • Aneurysm / genetics
  • Aneurysm / pathology
  • Glycogen Synthase Kinase 3 beta / genetics*
  • Humans
  • Lung Injury / genetics
  • Lung Injury / pathology
  • Macrophages / metabolism
  • Macrophages / pathology
  • Myocarditis / genetics*
  • Myocarditis / pathology
  • Polycystic Kidney Diseases / genetics*
  • Polycystic Kidney Diseases / pathology

Substances

  • GSK3B protein, human
  • Glycogen Synthase Kinase 3 beta