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Arch Pharm Res. 2019 Aug 1. doi: 10.1007/s12272-019-01177-2. [Epub ahead of print]

Filtering through the role of NRF2 in kidney disease.

Author information

1
Department of Pharmacology and Toxicology, University of Arizona, Tucson, AZ, USA.
2
Department of Pharmacology and Toxicology, University of Arizona, Tucson, AZ, USA. dzhang@pharmacy.arizona.edu.
3
University of Arizona Cancer Center, University of Arizona, Tucson, AZ, USA. dzhang@pharmacy.arizona.edu.

Abstract

Kidney disease affects ~‚ÄČ10% of the population worldwide, resulting in millions of deaths each year. Mechanistically, oxidative stress is a major driver of various kidney diseases, and promotes the progression from acute to chronic injury, as well as renal cancer development. NRF2, the master regulator of redox balance, has been shown to protect against kidney disease through its negation of reactive oxygen species (ROS). However, many kidney diseases exhibit high levels of ROS as a result of decreased NRF2 protein levels and transcriptional activity. Many studies have tested the strategy of using NRF2 inducing compounds to alleviate ROS to prevent or slow down the progression of kidney diseases. Oppositely, in specific subsets of renal cancer, NRF2 is constitutively activated and contributes to tumor burden and overall poor prognosis; therefore, there has been a recent interest in studies investigating the benefits of NRF2 inhibition. In this review, we summarize recent literature investigating the role of NRF2 and oxidative stress in various kidney diseases, and how pharmacological modification of NRF2 signaling could play a protective role.

KEYWORDS:

Hypertension; KEAP1; Kidney disease; NRF2; Oxidative stress; Renal cell carcinoma

PMID:
31372933
DOI:
10.1007/s12272-019-01177-2

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