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Area of Science:

  • Cellular Biology
  • Mitochondrial Biology
  • Biochemistry

Background:

  • Oxidative phosphorylation (OXPHOS) is a key metabolic process generating ATP.
  • Mitochondrial complex I activity during OXPHOS produces reactive oxygen species (ROS).
  • The antioxidant response element (ARE) pathway, regulated by NRF2, defends against oxidative stress.

Purpose of the Study:

  • To investigate the link between OXPHOS and the NRF2-mediated antioxidant response.
  • To elucidate the role of MAPK ERK5 in this pathway.
  • To determine if the antioxidant response to OXPHOS is ROS-dependent.

Main Methods:

  • Studied NRF2 expression and transcriptional activity in cells undergoing OXPHOS.
  • Investigated the role of MEF2 binding sites in the NRF2 promoter.
  • Utilized a mouse model to block OXPHOS and analyzed ERK5 and NRF2 expression.
  • Examined fibroblasts from patients with mitochondrial disorders.
  • Assessed the impact of mitochondrial complex I deficiency on ERK5 expression and ROS generation.

Main Results:

  • Cells performing OXPHOS showed induced NRF2 expression and activity.
  • MAPK ERK5 was found to induce MEF2-dependent NRF2 expression.
  • Blocking OXPHOS in mice reduced ERK5 and NRF2 levels.
  • Fibroblasts from mitochondrial disorder patients exhibited low ERK5 and NRF2 mRNA.
  • Cells lacking complex I activity failed to induce ERK5 and the antioxidant response during OXPHOS.
  • Complex I activity induces ERK5 via fumarate accumulation, independent of ROS.

Conclusions:

  • Eukaryotic cells possess a ROS-independent genetic program to prevent oxidative stress linked to OXPHOS.
  • The MAPK ERK5-MEF2-NRF2 pathway is crucial for this OXPHOS-induced antioxidant defense.
  • Mitochondrial dysfunction, particularly complex I defects, impairs this protective response.