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Dysregulation of Nrf2/Keap1 Redox Pathway in Diabetes Affects Multipotency of Stromal Cells

Piul S Rabbani1, Marc A Soares2, Sophia G Hameedi2

  • 1Hansjörg Wyss Department of Plastic Surgery, New York University School of Medicine, New York, NY piul.rabbani@nyumc.org daniel.ceradini@nyumc.org.

Diabetes
|October 25, 2018
PubMed

Insights

Diabetic bone marrow cells show impaired wound healing due to redox imbalance. Restoring the Nrf2/Keap1 pathway improves cell function and promotes diabetic wound repair.

Area of Science:

  • Biomedical Science
  • Cell Biology
  • Metabolic Research

Background:

  • Diabetes mellitus is characterized by metabolic dysregulation impacting cellular functions.
  • Reactive oxygen species (ROS) management is critical for cell integrity and wound healing.
  • Bone marrow-derived multipotent stromal cells (BMSCs) play a key role in tissue regeneration.

Purpose of the Study:

  • To investigate the role of redox signaling in diabetic BMSC regulation and function.
  • To identify molecular mechanisms underlying impaired wound healing in diabetes.
  • To explore therapeutic strategies targeting redox pathways in diabetic BMSCs.

Main Methods:

  • Comparative analysis of BMSCs from wild-type and diabetic mice.
  • Investigation of the nuclear factor erythroid-related factor 2 (Nrf2)/kelch-like erythroid cell-derived protein 1 (Keap1) pathway.
  • Manipulation of Nrf2/Keap1 signaling via Keap1 knockdown.
  • Assessment of BMSC multipotency and Sox2 expression.

Main Results:

  • Diabetic BMSCs exhibit dysregulated and insufficient Nrf2/Keap1 pathway activity.
  • Chronic ROS in diabetic BMSCs leads to altered metabolism and reduced multipotency.
  • Knockdown of Keap1 restores redox homeostasis and Nrf2/Keap1 signaling.
  • Restored signaling normalizes BMSC multipotency via Sox2 expression.

Conclusions:

  • The Nrf2/Keap1 pathway is a critical regulator of BMSC maintenance and differentiation, acting as a metabolic rheostat.
  • Dysregulation of Nrf2/Keap1 contributes to impaired wound healing in diabetes.
  • Targeting the Nrf2/Keap1 pathway offers translational potential for treating diabetic complications.

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