Targeting the KEAP1-NRF2 System to Prevent Kidney Disease Progression | Zendy

Masahiro Nezu | Zendy; Norio Suzuki | Zendy; Masayuki Yamamoto | Zendy

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Targeting the KEAP1-NRF2 System to Prevent Kidney Disease Progression

Author(s) -

Masahiro Nezu,

Norio Suzuki,

Masayuki Yamamoto

Publication year - 2017

Publication title -

american journal of nephrology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.394

H-Index - 85

eISSN - 1421-9670

pISSN - 0250-8095

DOI - 10.1159/000475890

Subject(s) - keap1 , oxidative stress , medicine , kidney disease , kidney , acute kidney injury , transcription factor , pharmacology , endocrinology , biology , biochemistry , gene

Nuclear factor erythroid 2-related factor 2 (NRF2) is a critical transcription factor for the antioxidative stress response and it activates a variety of cytoprotective genes related to redox and detoxification. NRF2 activity is regulated by the oxidative-stress sensor molecule Kelch-like ECH-associated protein 1 (KEAP1) that induces proteasomal degradation of NRF2 through ubiquitinating NRF2 under unstressed conditions. Because oxidative stress is a major pathogenic and aggravating factor for kidney diseases, the KEAP1-NRF2 system has been proposed to be a therapeutic target for renal protection.

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