Oxidative stress and chronic inflammation in osteoarthritis: can NRF2 counteract these partners in crime?
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 remo...
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| Veröffentlicht in: | Annals of the New York Academy of Sciences 2017-08, Vol.1401 (1), p.114-135 |
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| creator | Marchev, Andrey S. Dimitrova, Petya A. Burns, Andrew J. Kostov, Rumen V. Dinkova‐Kostova, Albena T. Georgiev, Milen I. |
| description | 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. |
| doi_str_mv | 10.1111/nyas.13407 |
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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.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>DOI: 10.1111/nyas.13407</identifier><identifier>PMID: 28662306</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Abnormalities ; Age ; Animals ; Arthritis ; Biocompatibility ; Bone remodeling ; Bone resorption ; Bone turnover ; Cartilage ; Cartilage diseases ; Chondrocytes - metabolism ; Chondrocytes - pathology ; Chronic Disease ; Crime ; Deformation mechanisms ; Humans ; Inflammation ; Inflammation - metabolism ; Inflammation - pathology ; Metabolism ; NF-E2-Related Factor 2 - metabolism ; NRF2 ; Nutrients ; Nutrition ; Osteoarthritis ; Osteoarthritis - metabolism ; Osteoarthritis - pathology ; Osteoblasts - metabolism ; Osteoblasts - pathology ; Oxidative stress ; Oxidative Stress - physiology ; Pain ; Pathology ; phytochemicals ; Protein Binding - physiology ; ROS ; Subchondral bone</subject><ispartof>Annals of the New York Academy of Sciences, 2017-08, Vol.1401 (1), p.114-135</ispartof><rights>2017 New York Academy of Sciences.</rights><rights>2017 The New York Academy of Sciences</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4197-e62f8b4357cb038e2b6583792225a9c31f58f5590862a94e305a73d190cfd7dc3</citedby><cites>FETCH-LOGICAL-c4197-e62f8b4357cb038e2b6583792225a9c31f58f5590862a94e305a73d190cfd7dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fnyas.13407$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fnyas.13407$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28662306$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marchev, Andrey S.</creatorcontrib><creatorcontrib>Dimitrova, Petya A.</creatorcontrib><creatorcontrib>Burns, Andrew J.</creatorcontrib><creatorcontrib>Kostov, Rumen V.</creatorcontrib><creatorcontrib>Dinkova‐Kostova, Albena T.</creatorcontrib><creatorcontrib>Georgiev, Milen I.</creatorcontrib><title>Oxidative stress and chronic inflammation in osteoarthritis: can NRF2 counteract these partners in crime?</title><title>Annals of the New York Academy of Sciences</title><addtitle>Ann N Y Acad Sci</addtitle><description>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.</description><subject>Abnormalities</subject><subject>Age</subject><subject>Animals</subject><subject>Arthritis</subject><subject>Biocompatibility</subject><subject>Bone remodeling</subject><subject>Bone resorption</subject><subject>Bone turnover</subject><subject>Cartilage</subject><subject>Cartilage diseases</subject><subject>Chondrocytes - metabolism</subject><subject>Chondrocytes - pathology</subject><subject>Chronic Disease</subject><subject>Crime</subject><subject>Deformation mechanisms</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Metabolism</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>NRF2</subject><subject>Nutrients</subject><subject>Nutrition</subject><subject>Osteoarthritis</subject><subject>Osteoarthritis - metabolism</subject><subject>Osteoarthritis - pathology</subject><subject>Osteoblasts - metabolism</subject><subject>Osteoblasts - pathology</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - physiology</subject><subject>Pain</subject><subject>Pathology</subject><subject>phytochemicals</subject><subject>Protein Binding - physiology</subject><subject>ROS</subject><subject>Subchondral bone</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1LJDEQhsOirLOze9kfIAEvIrTmo9NJvIiIroIo7MdhT00mXc1EupMxSe86_34zO-rBgzlUKOqpl6p6EfpKyTEt78SvTTqmvCbyA5pRWeuqaTjbQTNCpKyUZnwPfUrpgRDKVC0_oj2mmoZx0syQu39yncnuD-CUI6SEje-wXcbgncXO94MZx1IPviQ4pAzBxLyMLrt0iq3x-O77FcM2TD5DNDbjvIQEeFUoDzFtumx0I5x9Rru9GRJ8ef7n6NfV5c-L6-r2_tvNxfltZWuqZQUN69Wi5kLaBeEK2KIRikvNGBNGW057oXohNFENM7oGToSRvKOa2L6TneVzdLjVXcXwOEHK7eiShWEwHsKUWqqp4IIwSQt68AZ9CFP0ZbpCccmpEiXO0dGWsjGkFKFvV2UhE9ctJe3GgHZjQPvfgALvP0tOixG6V_Tl4gWgW-CvG2D9jlR79_v8x1b0H87OkB8</recordid><startdate>201708</startdate><enddate>201708</enddate><creator>Marchev, Andrey S.</creator><creator>Dimitrova, Petya A.</creator><creator>Burns, Andrew J.</creator><creator>Kostov, Rumen V.</creator><creator>Dinkova‐Kostova, Albena T.</creator><creator>Georgiev, Milen I.</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7ST</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>SOI</scope><scope>7X8</scope></search><sort><creationdate>201708</creationdate><title>Oxidative stress and chronic inflammation in osteoarthritis: can NRF2 counteract these partners in crime?</title><author>Marchev, Andrey S. ; 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| subjects | Abnormalities Age Animals Arthritis Biocompatibility Bone remodeling Bone resorption Bone turnover Cartilage Cartilage diseases Chondrocytes - metabolism Chondrocytes - pathology Chronic Disease Crime Deformation mechanisms Humans Inflammation Inflammation - metabolism Inflammation - pathology Metabolism NF-E2-Related Factor 2 - metabolism NRF2 Nutrients Nutrition Osteoarthritis Osteoarthritis - metabolism Osteoarthritis - pathology Osteoblasts - metabolism Osteoblasts - pathology Oxidative stress Oxidative Stress - physiology Pain Pathology phytochemicals Protein Binding - physiology ROS Subchondral bone |
| title | Oxidative stress and chronic inflammation in osteoarthritis: can NRF2 counteract these partners in crime? |
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