Molecular mechanisms of microglia- and astrocyte-driven neurorestoration triggered by application of electromagnetic fields

Croat Med J. 2019 Apr 30;60(2):127-140. doi: 10.3325/cmj.2019.60.127.

Abstract

Aim: To propose potential mechanisms of action of electromagnetic fields (EMF) on astrocytes and microglia and to elucidate the role of heat shock proteins (HSP), adenosine triphosphate (ATP), calcium ions (Ca2+), and hypoxia-inducible factor 1α (HIF1α) in neurorestoration following the application of EMF.

Methods: We reviewed the existing studies within the public domain and cross-evaluated their results in order to conclude on the molecular mechanisms of microglia-astrocyte crosstalk at work during EMF treatment.

Results: The existing studies suggest that EMF induces the increase of HSP70 expression and inhibition of HIF1α, thus decreasing inflammation and allowing the microglia-astrocyte crosstalk to initiate the formation of a glial scar within the central nervous system. Furthermore, by potentially up-regulating A2A and A3 adenosine receptors, EMF increases cAMP accumulation from astrocytes and reduces the expression of inflammatory cytokines TNF α and IL-8, thus initiating neurorestoration.

Conclusion: The microglia-astrocyte crosstalk during EMF treatment is crucial for the initiation of neurorestoration. Elucidating the exact mechanisms of EMF actions upon microglia and astrocytes, and its role in neurorestoration could be a key step in further research of the therapeutic potential of EMFs in various neurological disorders.

Publication types

  • Systematic Review

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Animals
  • Astrocytes / physiology*
  • Calcium / metabolism
  • Cells, Cultured
  • Cytokines
  • Electromagnetic Fields
  • Heat-Shock Proteins / metabolism
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Inflammation / metabolism
  • Inflammation / therapy
  • Magnetic Field Therapy*
  • Microglia / physiology*
  • Neurodegenerative Diseases / immunology
  • Neurodegenerative Diseases / therapy*
  • Receptor Cross-Talk
  • Tumor Necrosis Factor-alpha

Substances

  • Cytokines
  • Heat-Shock Proteins
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Tumor Necrosis Factor-alpha
  • Adenosine Triphosphate
  • Calcium