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      Chronic Inflammation in Chronic Kidney Disease Progression: Role of Nrf2

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          Abstract

          Despite recent advances in the management of chronic kidney disease (CKD), morbidity and mortality rates in these patients remain high. Although pressure-mediated injury is a well-recognized mechanism of disease progression in CKD, emerging data indicate that an intermediate phenotype involving chronic inflammation, oxidative stress, hypoxia, senescence, and mitochondrial dysfunction plays a key role in the etiology, progression, and pathophysiology of CKD. A variety of factors promote chronic inflammation in CKD, including oxidative stress and the adoption of a proinflammatory phenotype by resident kidney cells. Regulation of proinflammatory and anti-inflammatory factors through NF-κB– and nuclear factor, erythroid 2 like 2 (Nrf2)–mediated gene transcription, respectively, plays a critical role in the glomerular and tubular cell response to kidney injury. Chronic inflammation contributes to the decline in glomerular filtration rate (GFR) in CKD. Whereas the role of chronic inflammation in diabetic kidney disease (DKD) has been well-elucidated, there is now substantial evidence indicating unresolved inflammatory processes lead to fibrosis and eventual end-stage kidney disease (ESKD) in several other diseases, such as Alport syndrome, autosomal-dominant polycystic kidney disease (ADPKD), IgA nephropathy (IgAN), and focal segmental glomerulosclerosis (FSGS). In this review, we aim to clarify the mechanisms of chronic inflammation in the pathophysiology and disease progression across the spectrum of kidney diseases, with a focus on Nrf2.

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          Most cited references156

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          NF-κB signaling in inflammation

          The transcription factor NF-κB regulates multiple aspects of innate and adaptive immune functions and serves as a pivotal mediator of inflammatory responses. NF-κB induces the expression of various pro-inflammatory genes, including those encoding cytokines and chemokines, and also participates in inflammasome regulation. In addition, NF-κB plays a critical role in regulating the survival, activation and differentiation of innate immune cells and inflammatory T cells. Consequently, deregulated NF-κB activation contributes to the pathogenic processes of various inflammatory diseases. In this review, we will discuss the activation and function of NF-κB in association with inflammatory diseases and highlight the development of therapeutic strategies based on NF-κB inhibition.
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            Role of nrf2 in oxidative stress and toxicity.

            Qiang Ma (2013)
            Organismal life encounters reactive oxidants from internal metabolism and environmental toxicant exposure. Reactive oxygen and nitrogen species cause oxidative stress and are traditionally viewed as being harmful. On the other hand, controlled production of oxidants in normal cells serves useful purposes to regulate signaling pathways. Reactive oxidants are counterbalanced by complex antioxidant defense systems regulated by a web of pathways to ensure that the response to oxidants is adequate for the body's needs. A recurrent theme in oxidant signaling and antioxidant defense is reactive cysteine thiol-based redox signaling. The nuclear factor erythroid 2-related factor 2 (Nrf2) is an emerging regulator of cellular resistance to oxidants. Nrf2 controls the basal and induced expression of an array of antioxidant response element-dependent genes to regulate the physiological and pathophysiological outcomes of oxidant exposure. This review discusses the impact of Nrf2 on oxidative stress and toxicity and how Nrf2 senses oxidants and regulates antioxidant defense.
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              A Randomized Trial of Intensive versus Standard Blood-Pressure Control

              New England Journal of Medicine, 373(22), 2103-2116
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                Author and article information

                Contributors
                Journal
                Kidney Int Rep
                Kidney Int Rep
                Kidney International Reports
                Elsevier
                2468-0249
                04 May 2021
                July 2021
                04 May 2021
                : 6
                : 7
                : 1775-1787
                Affiliations
                [1 ]Department of Renal Medicine M99, Karolinska University Hospital at Huddinge, Karolinska Institutet, Stockholm, Sweden
                [2 ]Division of Nephrology, Stanford University, Stanford, California, USA
                [3 ]Department of Pediatrics, University of Cincinnati, Cincinnati, Ohio, USA
                [4 ]Department of Medicine, The University of British Columbia, Vancouver, Canada
                [5 ]Department of Pediatrics, Indiana University School of Medicine, Indiana University, Indianapolis, Indiana, USA
                [6 ]Division of Cardiology, New York University, New York, New York, USA
                [7 ]Division of Pediatric Nephrology, Children’s Mercy Kansas City, Kansas City, Missouri, USA
                Author notes
                [] Correspondence: Peter Stenvinkel, Department of Renal Medicine M99, Karolinska University Hospital at Huddinge, Karolinska Institutet, 141 86 Stockholm, Sweden. peter.stenvinkel@ 123456ki.se
                Article
                S2468-0249(21)01136-0
                10.1016/j.ekir.2021.04.023
                8258499
                34307974
                152300b3-2497-4edd-9a73-84fbb1c3215f
                © 2021 International Society of Nephrology. Published by Elsevier Inc.

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 15 March 2021
                : 13 April 2021
                : 19 April 2021
                Categories
                Review

                chronic inflammation,chronic kidney disease,mitochondrial dysfunction,nrf2,oxidative stress,resident kidney cells

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