Special Issue "Nrf2 in Kidney Injury and Physiology"
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: closed (1 July 2023) | Viewed by 7952
Acute kidney injury and progressive chronic kidney disease are debilitating diseases that can eventually lead to end-stage kidney disease. Acute kidney injury (AKI) has no effective treatment outside of supportive care, while treatment for the majority of CKD remains limited. The nuclear factor 2 erythroid 2 (NRF2) transcription factor is expressed in the kidney and upregulates cellular mechanisms involved in protection, including antioxidant responses, electrophile detoxifying genes, and anti-inflammatory effects. Its activity is restrained by Kelch-like ECH associated protein 1 (KEAP1) and glycogen synthase kinase 3 beta (GSK3B). Prior studies have demonstrated that NRF2 activity or enhancement protects against AKI, as well as AKI-to-CKD progression and interstitial fibrosis, suggesting a beneficial effect in the tubulointerstitial compartment of the kidney. However, the role of NRF2 in proteinuric glomerular diseases remains controversial. Some studies show that NRF2 reduces injury, while other studies demonstrate paradoxical increases in proteinuria and injury with NRF2 activation. Human trials show that NRF2 enhancers lead to short-term increases in glomerular filtration rate but can also worsen proteinuria. NRF2 has additional effects on renal salt and water handling and lipid metabolism. Additional research is required to determine the role of NRF2 in kidney physiology and disease, as well as the exact mechanisms of action for its effects. This Special Issue will highlight research that improves our understanding of NRF2 in the kidney.
Dr. Roderick Tan
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