The Connection Between Oxidative Stress, Mitochondrial Dysfunction, Iron Metabolism and Microglia in Multiple

Simonida Delic1, Svetlana Miletic Drakulic2, Milos Stepovic1

  • 1Department of Anatomy, Faculty of Medical Sciences Kragujevac, University of Kragujevac, 34000 Kragujevac, Serbia.

Neurosci
|March 26, 2025
PubMed

Insights

Mitochondrial dysfunction and iron metabolism in microglia are key in multiple sclerosis pathogenesis. This review highlights their roles in oxidative stress and neurodegeneration, shifting focus from neuroinflammation.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Mitochondrial dysfunction is increasingly implicated in multiple sclerosis (MS) pathogenesis.
  • Oxidative stress, a consequence of mitochondrial dysfunction, significantly impacts brain tissue in MS.
  • Microglia, the brain's immune cells, play a crucial role in clearing metabolites and iron, a known amplifier of oxidative stress.

Purpose of the Study:

  • To review current literature on oxidative stress, mitochondrial dysfunction, and iron metabolism in MS.
  • To elucidate the specific involvement of microglia in these interconnected processes within the context of MS.

Main Methods:

  • Literature review of recent studies on multiple sclerosis pathogenesis.
  • Analysis of research focusing on mitochondrial function, oxidative stress markers, and iron homeostasis.
  • Examination of microglial roles in metabolite and iron clearance in neurodegenerative diseases.

Main Results:

  • Emerging evidence links mitochondrial dysfunction and altered iron metabolism to MS.
  • Microglial activity in iron handling and metabolic clearance is critical.
  • Research focus is shifting towards neurodegeneration driven by these factors, rather than solely neuroinflammation.

Conclusions:

  • Oxidative stress, mitochondrial dysfunction, and iron metabolism are central to MS pathogenesis.
  • Microglia are key players mediating these processes and influencing neurodegeneration.
  • Understanding these mechanisms offers new therapeutic avenues for multiple sclerosis.