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      New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis

      review-article
      1 , 1 , * , , , , , , , *
      Redox Biology
      Elsevier
      ACC, acetyl-CoA carboxylase, AdipoR, adiponectin receptor, AGEs, advanced glycation end-products, AKR, aldo-keto reductase, AMPK, AMP-activated protein kinase, ApoE, apolipoprotein E, AR, aldose reductase, CAD, coronary artery disease, C/EBPα, CCAAT/enhancer binding protein α, CRP, C-reactive protein, CVD, cardiovascular disease, DAG, diacylglycerol, Drp-1, dynamic-related protein 1, eNOS, endothelial nitric oxide synthase, ERK1/2, extracellular regulating kinase 1/2, ER, endoplasmic reticulum, FOXO1, forkhead box O1, GAPDH, glyceraldehydes-3-phosphate dehydrogenase, GLP-1, glucagon-like peptide-1, Grxs, glutaredoxins, GSH, glutathione, H2S, hydrogen sulphide, HDL, high-density lipoprotein cholesterol, HIF-α, hypoxia inducible factor α, IKK, IkB kinase, ICAM-1, intercellular adhesion molecule-1, IκB, inhibitor of κB, IL-6, interleukin-6, iNOS, inducible NOS, JNK, c-Jun N-terminal kinase, KLF, Kruppel-like factors, LPS, lipopolysaccharide, MAPK, mitogen-activated protein kinase, MCP-1, monocyte chemotactic protein-1, MIP-1, macrophage inflammatory protein-1, miRNAs, microRNAs, miR-128-1, miRNA-128-1, MMPs, matrix metalloproteinases, NF-κB, nuclear factor-κB, NLRP3, NOD-like receptor family, pyrin domain-containing 3, nNOS, neuronal NOS, Nrf2, nuclear factor erythoid 2-related factor 2, ox-LDL, oxidized-low density lipoprotein, PARP, poly ADP-ribose polymerase, PGC-1α, PPARγ coactivator 1 α, PKC, protein kinase C, p90RSK, p90 ribosomal S6 kinase, PPAR, peroxisome proliferator activated receptor, RAGE, receptor for AGEs, ROS, reactive oxygen species, SIRT1, sirtuin 1, SREBP-1c, sterol regulatory-element-binding protein-1c, SR, scavenger receptor, SUMOylation, small ubiquitin-related modifier conjugation, TLR4, toll-like receptor 4, TMAO, trimethylamine N-oxide, TNF-α, tumor necrosis factor-α, T2DM, Type 2 diabetes mellitus, UPS, ubiquitin-proteasome system, VCAM-1, vascular cell adhesion molecule 1, VSMCs, vascular smooth muscle cells, Atherosclerosis, Diabetes mellitus, Reactive oxygen species, Gut microbiota, MicroRNA

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          Abstract

          Oxidative stress and inflammation interact in the development of diabetic atherosclerosis. Intracellular hyperglycemia promotes production of mitochondrial reactive oxygen species (ROS), increased formation of intracellular advanced glycation end-products, activation of protein kinase C, and increased polyol pathway flux. ROS directly increase the expression of inflammatory and adhesion factors, formation of oxidized-low density lipoprotein, and insulin resistance. They activate the ubiquitin pathway, inhibit the activation of AMP-protein kinase and adiponectin, decrease endothelial nitric oxide synthase activity, all of which accelerate atherosclerosis. Changes in the composition of the gut microbiota and changes in microRNA expression that influence the regulation of target genes that occur in diabetes interact with increased ROS and inflammation to promote atherosclerosis. This review highlights the consequences of the sustained increase of ROS production and inflammation that influence the acceleration of atherosclerosis by diabetes. The potential contributions of changes in the gut microbiota and microRNA expression are discussed.

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          Most cited references163

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          Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions.

          Adiponectin plays a central role as an antidiabetic and antiatherogenic adipokine. AdipoR1 and AdipoR2 serve as receptors for adiponectin in vitro, and their reduction in obesity seems to be correlated with reduced adiponectin sensitivity. Here we show that adenovirus-mediated expression of AdipoR1 and R2 in the liver of Lepr(-/-) mice increased AMP-activated protein kinase (AMPK) activation and peroxisome proliferator-activated receptor (PPAR)-alpha signaling pathways, respectively. Activation of AMPK reduced gluconeogenesis, whereas expression of the receptors in both cases increased fatty acid oxidation and lead to an amelioration of diabetes. Alternatively, targeted disruption of AdipoR1 resulted in the abrogation of adiponectin-induced AMPK activation, whereas that of AdipoR2 resulted in decreased activity of PPAR-alpha signaling pathways. Simultaneous disruption of both AdipoR1 and R2 abolished adiponectin binding and actions, resulting in increased tissue triglyceride content, inflammation and oxidative stress, and thus leading to insulin resistance and marked glucose intolerance. Therefore, AdipoR1 and R2 serve as the predominant receptors for adiponectin in vivo and play important roles in the regulation of glucose and lipid metabolism, inflammation and oxidative stress in vivo.
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            Oxygen radicals, nitric oxide, and peroxynitrite: Redox pathways in molecular medicine

            Aerobic life in humans imposes the hazard of excess oxidation in cell and tissue components that may compromise cell function and viability. The formation and accumulation of oxidized products in biomolecules such as proteins and lipids are observed in various pathologies and during the normal aging process. This review article aims to integrate some early and remarkable discoveries in the field, with more recent developments that helped to define a causative role of oxygen radicals, nitric oxide, and peroxynitrite in human physiology and pathology. These aspects of human redox biochemistry contribute to the understanding of the molecular basis of diseases and aging and open avenues for the development of preventive and therapeutic strategies in molecular medicine. Oxygen-derived free radicals and related oxidants are ubiquitous and short-lived intermediates formed in aerobic organisms throughout life. These reactive species participate in redox reactions leading to oxidative modifications in biomolecules, among which proteins and lipids are preferential targets. Despite a broad array of enzymatic and nonenzymatic antioxidant systems in mammalian cells and microbes, excess oxidant formation causes accumulation of new products that may compromise cell function and structure leading to cell degeneration and death. Oxidative events are associated with pathological conditions and the process of normal aging. Notably, physiological levels of oxidants also modulate cellular functions via homeostatic redox-sensitive cell signaling cascades. On the other hand, nitric oxide ( • NO), a free radical and weak oxidant, represents a master physiological regulator via reversible interactions with heme proteins. The bioavailability and actions of • NO are modulated by its fast reaction with superoxide radical ( O 2 • − ), which yields an unusual and reactive peroxide, peroxynitrite, representing the merging of the oxygen radicals and • NO pathways. In this Inaugural Article, I summarize early and remarkable developments in free radical biochemistry and the later evolution of the field toward molecular medicine; this transition includes our contributions disclosing the relationship of • NO with redox intermediates and metabolism. The biochemical characterization, identification, and quantitation of peroxynitrite and its role in disease processes have concentrated much of our attention. Being a mediator of protein oxidation and nitration, lipid peroxidation, mitochondrial dysfunction, and cell death, peroxynitrite represents both a pathophysiologically relevant endogenous cytotoxin and a cytotoxic effector against invading pathogens.
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              Brown remodeling of white adipose tissue by SirT1-dependent deacetylation of Pparγ.

              Brown adipose tissue (BAT) can disperse stored energy as heat. Promoting BAT-like features in white adipose (WAT) is an attractive, if elusive, therapeutic approach to staunch the current obesity epidemic. Here we report that gain of function of the NAD-dependent deacetylase SirT1 or loss of function of its endogenous inhibitor Deleted in breast cancer-1 (Dbc1) promote "browning" of WAT by deacetylating peroxisome proliferator-activated receptor (Ppar)-γ on Lys268 and Lys293. SirT1-dependent deacetylation of Lys268 and Lys293 is required to recruit the BAT program coactivator Prdm16 to Pparγ, leading to selective induction of BAT genes and repression of visceral WAT genes associated with insulin resistance. An acetylation-defective Pparγ mutant induces a brown phenotype in white adipocytes, whereas an acetylated mimetic fails to induce "brown" genes but retains the ability to activate "white" genes. We propose that SirT1-dependent Pparγ deacetylation is a form of selective Pparγ modulation of potential therapeutic import. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Redox Biol
                Redox Biol
                Redox Biology
                Elsevier
                2213-2317
                19 October 2018
                January 2019
                19 October 2018
                : 20
                : 247-260
                Affiliations
                [0005]The School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China
                Author notes
                [1]

                These authors contributed equally to this work.

                Article
                S2213-2317(18)30737-7
                10.1016/j.redox.2018.09.025
                6205410
                30384259
                15ceead8-ec6d-4a6c-9ed7-adf59c19055e
                © 2018 The Authors

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

                History
                : 15 August 2018
                : 12 September 2018
                : 29 September 2018
                Categories
                Review Article

                acc, acetyl-coa carboxylase,adipor, adiponectin receptor,ages, advanced glycation end-products,akr, aldo-keto reductase,ampk, amp-activated protein kinase,apoe, apolipoprotein e,ar, aldose reductase,cad, coronary artery disease,c/ebpα, ccaat/enhancer binding protein α,crp, c-reactive protein,cvd, cardiovascular disease,dag, diacylglycerol,drp-1, dynamic-related protein 1,enos, endothelial nitric oxide synthase,erk1/2, extracellular regulating kinase 1/2,er, endoplasmic reticulum,foxo1, forkhead box o1,gapdh, glyceraldehydes-3-phosphate dehydrogenase,glp-1, glucagon-like peptide-1,grxs, glutaredoxins,gsh, glutathione,h2s, hydrogen sulphide,hdl, high-density lipoprotein cholesterol,hif-α, hypoxia inducible factor α,ikk, ikb kinase,icam-1, intercellular adhesion molecule-1,iκb, inhibitor of κb,il-6, interleukin-6,inos, inducible nos,jnk, c-jun n-terminal kinase,klf, kruppel-like factors,lps, lipopolysaccharide,mapk, mitogen-activated protein kinase,mcp-1, monocyte chemotactic protein-1,mip-1, macrophage inflammatory protein-1,mirnas, micrornas,mir-128-1, mirna-128-1,mmps, matrix metalloproteinases,nf-κb, nuclear factor-κb,nlrp3, nod-like receptor family, pyrin domain-containing 3,nnos, neuronal nos,nrf2, nuclear factor erythoid 2-related factor 2,ox-ldl, oxidized-low density lipoprotein,parp, poly adp-ribose polymerase,pgc-1α, pparγ coactivator 1 α,pkc, protein kinase c,p90rsk, p90 ribosomal s6 kinase,ppar, peroxisome proliferator activated receptor,rage, receptor for ages,ros, reactive oxygen species,sirt1, sirtuin 1,srebp-1c, sterol regulatory-element-binding protein-1c,sr, scavenger receptor,sumoylation, small ubiquitin-related modifier conjugation,tlr4, toll-like receptor 4,tmao, trimethylamine n-oxide,tnf-α, tumor necrosis factor-α,t2dm, type 2 diabetes mellitus,ups, ubiquitin-proteasome system,vcam-1, vascular cell adhesion molecule 1,vsmcs, vascular smooth muscle cells,atherosclerosis,diabetes mellitus,reactive oxygen species,gut microbiota,microrna
                acc, acetyl-coa carboxylase, adipor, adiponectin receptor, ages, advanced glycation end-products, akr, aldo-keto reductase, ampk, amp-activated protein kinase, apoe, apolipoprotein e, ar, aldose reductase, cad, coronary artery disease, c/ebpα, ccaat/enhancer binding protein α, crp, c-reactive protein, cvd, cardiovascular disease, dag, diacylglycerol, drp-1, dynamic-related protein 1, enos, endothelial nitric oxide synthase, erk1/2, extracellular regulating kinase 1/2, er, endoplasmic reticulum, foxo1, forkhead box o1, gapdh, glyceraldehydes-3-phosphate dehydrogenase, glp-1, glucagon-like peptide-1, grxs, glutaredoxins, gsh, glutathione, h2s, hydrogen sulphide, hdl, high-density lipoprotein cholesterol, hif-α, hypoxia inducible factor α, ikk, ikb kinase, icam-1, intercellular adhesion molecule-1, iκb, inhibitor of κb, il-6, interleukin-6, inos, inducible nos, jnk, c-jun n-terminal kinase, klf, kruppel-like factors, lps, lipopolysaccharide, mapk, mitogen-activated protein kinase, mcp-1, monocyte chemotactic protein-1, mip-1, macrophage inflammatory protein-1, mirnas, micrornas, mir-128-1, mirna-128-1, mmps, matrix metalloproteinases, nf-κb, nuclear factor-κb, nlrp3, nod-like receptor family, pyrin domain-containing 3, nnos, neuronal nos, nrf2, nuclear factor erythoid 2-related factor 2, ox-ldl, oxidized-low density lipoprotein, parp, poly adp-ribose polymerase, pgc-1α, pparγ coactivator 1 α, pkc, protein kinase c, p90rsk, p90 ribosomal s6 kinase, ppar, peroxisome proliferator activated receptor, rage, receptor for ages, ros, reactive oxygen species, sirt1, sirtuin 1, srebp-1c, sterol regulatory-element-binding protein-1c, sr, scavenger receptor, sumoylation, small ubiquitin-related modifier conjugation, tlr4, toll-like receptor 4, tmao, trimethylamine n-oxide, tnf-α, tumor necrosis factor-α, t2dm, type 2 diabetes mellitus, ups, ubiquitin-proteasome system, vcam-1, vascular cell adhesion molecule 1, vsmcs, vascular smooth muscle cells, atherosclerosis, diabetes mellitus, reactive oxygen species, gut microbiota, microrna

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