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Reductive stress impairs myogenic differentiation.

Namakkal S Rajasekaran1, Sandeep Balu Shelar2, Dean P Jones3

  • 1Cardiac Aging & Redox Signaling Laboratory, Molecular and Cellular Pathology, Department of Pathology, Birmingham, AL, USA; Division of Cardiovascular Medicine, Department of Medicine, University of Utah School of Medicine, Salt Lake City, UT, USA; Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA.

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Summary
This summary is machine-generated.

Activating Nrf2 signaling to combat oxidative stress surprisingly inhibits skeletal muscle regeneration. Over-activation leads to reductive stress, impairing myoblast differentiation and muscle repair.

Keywords:
Differentiation markersNrf2-signalingPro-oxidative settingReactive oxygen species (ROS)Reductive stressSatellite cellsSkeletal muscle regeneration

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Area of Science:

  • Muscle regeneration and cellular redox homeostasis.
  • Molecular mechanisms of skeletal muscle differentiation.
  • Role of Nrf2 signaling in cellular stress responses.

Background:

  • Skeletal muscle regeneration relies on myo-satellite cells differentiating into muscle fibers.
  • Oxidative stress at injury sites can impair muscle regeneration.
  • Previous work showed Nrf2/antioxidant signaling abrogation impairs skeletal muscle regeneration.

Purpose of the Study:

  • To investigate if activating intracellular Nrf2 signaling promotes antioxidant transcription and myoblast differentiation.
  • To determine the effects of sulforaphane-induced Nrf2 activation on C2C12 myoblast differentiation.

Main Methods:

  • C2C12 myoblasts were treated with sulforaphane (SF) to activate Nrf2 signaling.
  • Gene expression of Nrf2-antioxidants (GCLC, G6PD) and differentiation markers (MyoD, Pax7, Myh2) were analyzed.
  • Effects of N-acetyl-cysteine (NAC), GSH-ester, and Keap1 knockdown on differentiation were assessed.

Main Results:

  • SF treatment increased Nrf2-antioxidant expression and reduced glutathione (GSH) production, creating a reductive redox state.
  • This reductive state significantly inhibited myoblast differentiation, evidenced by morphological changes and reduced marker expression.
  • NAC, GSH-ester, and Keap1 knockdown also induced reductive stress and inhibited differentiation.

Conclusions:

  • Over-activation of Nrf2 signaling leads to reductive stress, which hampers skeletal muscle satellite cell differentiation.
  • Disrupting physiological reactive oxygen species (ROS) signaling by inducing reductive stress impairs muscle regeneration.
  • Modulating Nrf2 activation is crucial for effective muscle repair, as excessive activation is detrimental.