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Keap1 inhibition attenuates glomerulosclerosis.

Yoichi Miyazaki1, Akihiro Shimizu, Ira Pastan

  • 1Division of Kidney and Hypertension, Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|February 14, 2014
PubMed
Summary

Inhibition of Kelch-like ECH-associated protein 1 (Keap1) activates NFE2-related factor 2 (Nrf2), protecting against glomerulosclerosis in podocyte injury models. This suggests the Nrf2-Keap1 system is a viable therapeutic target for chronic kidney diseases.

Keywords:
antioxidant genesglomerulosclerosishypomorphic alleleoxidative stress

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Genetics

Background:

  • NFE2-related factor 2 (Nrf2) is a key regulator of antioxidant genes.
  • Kelch-like ECH-associated protein 1 (Keap1) inhibits Nrf2; its inhibition activates Nrf2.
  • Podocyte injury leads to glomerulosclerosis, a progressive kidney disease.

Purpose of the Study:

  • To investigate the impact of modulating the Keap1-Nrf2 system on podocyte injury and glomerulosclerosis.
  • To determine if Keap1 knockdown affects Nrf2 activation and subsequent kidney damage.

Main Methods:

  • Nrf2 knockout and Keap1 hypomorphic knockdown mice were crossed with NEP25 mice to induce podocyte-specific injury.
  • Analysis of oxidative stress markers, Nrf2 target gene expression, and kidney injury markers.

Main Results:

  • Keap1 knockdown upregulated Nrf2 target genes in glomeruli.
  • Podocyte injury did not activate Nrf2 in Keap1 wild-type mice.
  • Keap1 knockdown significantly attenuated glomerulosclerosis and preserved podocyte integrity.

Conclusions:

  • Podocyte injury is ineffective at activating Nrf2.
  • Nrf2 activation via Keap1 knockdown ameliorates glomerulosclerosis.
  • The Nrf2-Keap1 pathway represents a promising therapeutic target for chronic kidney diseases.