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Keap1 hypomorphism protects against ischemic and obstructive kidney disease
Roderick J Tan1, Dionysios V Chartoumpekis2, Brittney M Rush1
1Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Scientific Reports
|November 3, 2016
Summary
The Keap1/Nrf2 pathway protects against kidney disease. Hyperactivating this pathway in mice improved recovery from kidney injury and reduced fibrosis, demonstrating its therapeutic potential.
Area of Science:
- Nephrology
- Molecular Biology
- Immunology
Background:
- The Keap1/Nrf2 pathway is crucial for cellular defense against oxidative stress and inflammation.
- Dysregulation of this pathway is implicated in various kidney diseases.
- Understanding its role is vital for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the protective role of the Keap1/Nrf2 pathway in kidney injury models.
- To evaluate the therapeutic potential of Nrf2 hyperactivation in kidney disease.
Main Methods:
- Utilized Keap1 hypomorphic mice with Nrf2 hyperactivation and wild-type controls.
- Induced kidney injury using ischemia/reperfusion injury (IRI) and unilateral ureteral obstruction (UUO) models.
- Assessed tubular injury, serum creatinine, renal fibrosis, and expression of Nrf2-regulated genes (GSTM1, GSTP1, NQO1).
Main Results:
- Keap1 hypomorphic mice showed improved serum creatinine levels and attenuated renal fibrosis post-IRI.
- Nrf2 target gene expression was higher at baseline and less suppressed post-injury in hypomorphs.
- Significant protection and increased Nrf2 target gene expression were observed in hypomorphs following UUO.
Conclusions:
- Nrf2 hyperactivation confers significant protection against diverse kidney injuries, including IRI and UUO.
- The Keap1/Nrf2 pathway plays a critical cytoprotective role in the kidney.
- Targeting the Nrf2 pathway holds promise for treating kidney diseases.
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