Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1865, Issue 5, Pages 721-733Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2018.02.010
Keywords
Nrf2/Keap1; Antioxidant system; Striated muscle; Oxidative stress; Reductive stress; Nrf2/NF-kappa B cross-talk; Autophagy
Categories
Funding
- Fondazione Cassa di Risparmio di Perugia [CRP2015-0326.021, CRP 2016-0136.021]
- Ministero dell'Istruzione, dell'Universita e della Ricerca, Italy [PRIN 2010R8JK2X_004, FIRB RBFR12BUMH]
- Association Francaise contre les Myopathies [16812]
- Associazione Italiana per la Ricerca sul Cancro [17581]
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Nrf2 and its endogenous inhibitor, Keap1, function as a ubiquitous, evolutionarily conserved intracellular defense mechanism to counteract oxidative stress. Sequestered by cytoplasmic Keap1 and targeted to proteasomal degradation in basal conditions, in case of oxidative stress Nrf2 detaches from Keap1 and translocates to the nucleus, where it heterodimerizes with one of the small Maf proteins. The heterodimers recognize the AREs, that are enhancer sequences present in the regulatory regions of Nrf2 target genes, essential for the recruitment of key factors for transcription. In the present review we briefly introduce the Nrf2-Keap1 system and describe Nrf2 functions, illustrate the Nrf2-NF-kappa B cross-talk, and highlight the effects of the Nrf2-Keap1 system in the physiology and pathophysiology of striated muscle tissue taking into account its role(s) in oxidative stress and reductive stress.
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