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The Keap1/Nrf2 Signaling Pathway in the Thyroid-2020 Update

Christina Thanas1, Panos G Ziros1, Dionysios V Chartoumpekis1,2

  • 1Service of Endocrinology, Diabetology and Metabolism, Lausanne University Hospital and University of Lausanne, CH-1011 Lausanne, Switzerland.

Antioxidants (Basel, Switzerland)
|November 7, 2020
PubMed

Insights

The thyroid gland uniquely produces and defends against reactive oxygen species (ROS). The Keap1/Nrf2 pathway is crucial for thyroid homeostasis and is implicated in various thyroid diseases.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cellular Physiology

Background:

  • The thyroid gland has a dual role concerning reactive oxygen species (ROS): it defends against them and produces them for hormone synthesis.
  • Maintaining thyroid homeostasis requires robust antioxidant defense systems due to continuous self-exposure to ROS.
  • The Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, inhibited by Kelch-like ECH-associated protein 1 (Keap1), is a key endogenous antioxidant system.

Purpose of the Study:

  • To review recent findings on the role of the Keap1/Nrf2 signaling pathway in thyroid physiology.
  • To explore the involvement of Keap1/Nrf2 signaling in various thyroid pathologies.

Main Methods:

  • Literature review of recent studies.
  • Analysis of research linking Keap1/Nrf2 signaling to thyroid function and disease.

Main Results:

  • Emerging evidence highlights significant links between the Keap1/Nrf2 pathway and thyroid physiology.
  • The Keap1/Nrf2 pathway is implicated in thyroid conditions such as autoimmunity, goiter, hypothyroidism, hyperthyroidism, and cancer.

Conclusions:

  • The Keap1/Nrf2 pathway plays a critical role in regulating thyroid homeostasis.
  • Dysregulation of Keap1/Nrf2 signaling is associated with the development and progression of thyroid diseases.
Keywords:
Keap1 (Kelch-like ECH-associated protein 1)Nrf2 (nuclear factor erythroid 2-related factor 2)antioxidantgoiteroxidative stressthyroglobulinthyroid

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