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Oxidative stress and chronic inflammation in osteoarthritis: can NRF2 counteract these partners in crime?
Author(s) -
Marchev Andrey S.,
Dimitrova Petya A.,
Burns Andrew J.,
Kostov Rumen V.,
DinkovaKostova Albena T.,
Georgiev Milen I.
Publication year - 2017
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.13407
Subject(s) - oxidative stress , inflammation , osteoarthritis , bone remodeling , cartilage , medicine , osteoclast , disease , transcription factor , bone resorption , pathology , bioinformatics , cancer research , biology , anatomy , genetics , gene , alternative medicine , receptor
Osteoarthritis (OA) is an age‐related joint degenerative disease associated with pain, joint deformity, and disability. The disease starts with cartilage damage but then progressively involves subchondral bone, causing an imbalance between osteoclast‐driven bone resorption and osteoblast‐driven remodeling. Here, we summarize the data for the role of oxidative stress and inflammation in OA pathology and discuss how these two processes are integrated during OA progression, as well as their contribution to abnormalities in cartilage/bone metabolism and integrity. At the cellular level, oxidative stress and inflammation are counteracted by transcription factor nuclear factor erythroid p45–related factor 2 (NRF2), and we describe the regulation of NRF2, highlighting its role in OA pathology. We also discuss the beneficial effect of some phytonutrients, including the therapeutic potential of NRF2 activation, in OA.