氧化应激相关心血管疾病与NF-κB信号通路关系的研究现状
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摘要
氧化应激与多种心血管疾病相关,在病理情况下,机体的氧自由基过量生成或抗氧化防御系统受损,蓄积的活性氧(Reactive oxygen species,ROS)除了对细胞产生直接的损害外还可以激活多种信号通路,间接导致组织损伤,如促使心力衰竭、糖尿病、动脉粥样硬化发生。近年来氧化应激与NF-κB信号通路的相关研究越来越受关注。本文就氧化应激相关心血管疾病与NF-κB信号通路关系的研究进行综述。
Oxidative stress is associated with a variety of cardiovascular diseases. In pathological conditions,the oxygen free radicals in the body are overproduced or the antioxidant defense system is damaged. In addition to direct damage to cells,accumulation of reactive oxygen species( ROS) activates a variety of signaling pathways and causes tissue damage indirectly,such as heart failure,diabetes mellitus,and atherosclerosis. The research of oxidative stress and NF-κB signaling pathway has attracted more and more attention in recent years. This article reviews the research on the relationship between oxidative stress-related cardiovascular diseases and NF-κB signaling pathway.
Oxidative stress is associated with a variety of cardiovascular diseases. In pathological conditions,the oxygen free radicals in the body are overproduced or the antioxidant defense system is damaged. In addition to direct damage to cells,accumulation of reactive oxygen species( ROS) activates a variety of signaling pathways and causes tissue damage indirectly,such as heart failure,diabetes mellitus,and atherosclerosis. The research of oxidative stress and NF-κB signaling pathway has attracted more and more attention in recent years. This article reviews the research on the relationship between oxidative stress-related cardiovascular diseases and NF-κB signaling pathway.
引文
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[35]Yang J,Li Y,Hu C.Ischemic preconditioning protects against myocardial,ischemia-reperfusion injury through,inhibiting toll-like receptor 4/NF-κB signaling pathway in rats[J].Journal of Central South University,2011,36(10):972.
[36]Kawano S,Kubota T,Monden Y,et al.Blockade of NFkappa B improves cardiac function and survival after myocardial infarction[J].American Journal of Physiology Heart&Circulatory Physiology,2006,291(3):1337-44.
[37]Ling H,Gray C B,Zambon A,et al.Cardiomyocytespecific p65 NF-kappa B deletion protects the injured heart by preservation of calcium handling[J].Am J Physiol Heart Circ Physiol,2013,305(7):1089-97.
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[39]Li T,Yu J,Chen R,et al.Mycophenolate mofetil attenuates myocardial ischemia-reperfusion injury via regulation of the TLR4/NF-B signaling pathway[J].Die Pharmazie,2014,69(11):850-5.
[40]Nishida K,Otsu K.Autophagy during cardiac remodeling[J].Journal of Molecular&Cellular Cardiology,2015,95:11-18.
[41]梁逸强,潘朝锌,何新兵,等.心室重构防治研究的进展[J].心血管康复医学杂志,2013,22(4):425-428.
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[44]Patel N.The effect of antisense to NF-kappa B in an albumin microsphere formulation on the progression of left-ventricular remodeling associated with chronic volume overload in rats[J].J Drug Target,2014,22(9):796-804.
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[46]Onai Y.Inhibition of NF-kappa B improves left ventricular remodeling and cardiac dysfunction after myocardial infarction[J].Am J Physiol Heart Circ Physiol,2007,292(1):530-8.
[47]Zelarayan L.NF-kappa B activation is required for adaptive cardiac hypertrophy[J].Cardiovasc Res,2009,84(3):416-24.
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[2]Sverdlov A L,Elezaby A,Qin F,et al.Mitochondrial Reactive Oxygen Species Mediate Cardiac Structural,Functional,and Mitochondrial Consequences of Diet-Induced Metabolic Heart Disease[J].Journal of the American Heart Association,2016,5(1):919-24.
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[4]Jiang C,Tong YL,Zhang D,et al.Sinomenine prevents the development of cardiomyopathy in diabetic rats by inhibiting inflammatory responses and blocking activation of NF-κB[J].General physiology and biophysics,2017,36(1):65-74.
[5]Xu X,Si L,Xu J,et al.Asiatic acid inhibits cardiac hypertrophy by blocking interleukin-1β-activated nuclear factor-κB signaling in vitro and in vivo[J].Journal of Thoracic Disease,2015,7(10):1787-1797.
[6]Xu T,Li T,Yang F,et al.Exercise preconditioning attenuates pressure overload-induced pathological cardiac hypertrophy:potential role of HSF1 and NF-κB p65 signaling[J].Zhonghua xin xue guan bing za zhi,2015,43(10):894-899.
[7]Xu T,Zhang B,Yang F,et al.HSF1 and NF-κB p65participate in the process of exercise preconditioning attenuating pressure overload-induced pathological cardiac hypertrophy[J].Biochemical&Biophysical Research Communications,2015,460(3):622-7.
[8]Queisser N,Schupp N.Aldosterone,oxidative stress,and NF-κB activation in hypertension-related cardiovascular and renal diseases[J].Free Radical Biology&Medicine,2012,53(2):314-327.
[9]Tham Y K,Bernardo B C,Ooi J Y Y,et al.Pathophysiology of cardiac hypertrophy and heart failure:signaling pathways and novel therapeutic targets[J].Archives of Toxicology,2015,89(9):1401-38.
[10]陈榕,夏中元,孟庆涛,等.氧化应激过程中信号转导通路的研究进展[J].山东医药,2015(29):98-100.
[11]Zhang J,Wang X,Vikash V,et al.ROS and ROS-Mediated Cellular Signaling[J].Oxidative Medicine&Cellular Longevity,2016,2016:5782.
[12]Heiden K V D,Cuhlmann S,Luong L A,et al.Role of nuclear factorκB in cardiovascular health and disease[J].Clinical Science,2010,118(10):593-605.
[13]Hinz,M.and C.Scheidereit,The Ikappa B kinase complex in NF-kappa B regulation and beyond[J].EMBO Rep,2014,15(1):46-61.
[14]吴建利,李家富,冯健.核因子-κB在心室重构中的研究进展[J].心血管病学进展,2015(6):756-759.
[15]Fu J,Shi Q,Song X,et al.Tetrachlorobenzoquinone exhibits neurotoxicity by inducing inflammatory responses through ROS mediated IKK/IκB/NF-κB signaling[J].Environmental Toxicology Pharmacology,2015,41:241-250.
[16]Yu X,Hong F,Zhang Y Q.Cardiac inflammation involving in PKC or ERK1/2-activated NF-κB signalling pathway in mice following exposure to titanium dioxide nanoparticles[J].Journal of Hazardous Materials,2016,313:68-77.
[17]郭金昊,姜月华,杨传华.核转录因子NF-κB在心血管疾病中作用的研究进展[J].中西医结合心脑血管病杂志,2016,14(11):1227-1230.
[18]Heiden K V D,Cuhlmann S,Luong L A,et al.Role of nuclear factorκB in cardiovascular health and disease[J].Clinical Science,2010,118(10):593-605.
[19]葛均波,徐永健.内科学[M].第8版.北京:人民卫生出版社,2013:220-227.
[20]Cosentino F,Hürlimann D,Delli G C,et al.Chronic treatment with tetrahydrobiopterin reverses endothelial dysfunction and oxidative stress in hypercholesterolaemia[J].Heart,2008,94(4):487-492.
[21]Pierce G L,Lesniewski L A,Lawson B R,et al.Nuclear factor-kappa B activation contributes to vascular endothelial dysfunction via oxidative stress in overweight/obese middle-aged and older humans[J].Circulation,2009,119(9):1284.
[22]张芯.核因子-κB在动脉粥样硬化中的研究进展[J].现代生物医学进展,2015(5):972-975.
[23]Lamon B D,Hajjar D P.Inflammation at the molecular interface of atherogenesis:an anthropological journey[J].American Journal of Pathology,2008,173(5):1253.
[24]Kutuk O,Basaga H.Inflammation meets oxidation:NFkappa B as a mediator of initial lesion development in atherosclerosis[J].Trends in Molecular Medicine,2003,9(12):549.
[25]Pateras I,Giaginis C,Tsigris C,et al.NF-κB signaling at the crossroads of inflammation and atherogenesis:searching for new therapeutic links[J].Expert Opinion on Therapeutic Targets,2014,18(9):1089.
[26]Kanters E,Pasparakis M,Gijbels M J J,et al.Inhibition of NF-κB activation in macrophages increases atherosclerosis in LDL receptor-deficient mice[J].Journal of Clinical Investigation,2003,112(8):1176-1185.
[27]Brown,Jonathan,Lin,et al.NF-κB Directs Dynamic Super Enhancer Formation in Inflammation and Atherogenesis[J].Molecular Cell,2014,56(2):219.
[28]Wu B,Lin R,Dai R,et al.Valsartan attenuates oxidative stress and NF-κB activation and reduces myocardial apoptosis after ischemia and reperfusion[J].european journal of pharmacology,2013,705:140-147
[29]Cummins E P,Berra E,Comerford K M,et al.Prolyl hydroxylase-1 negatively regulates IκB kinase-β,giving insight into hypoxia-induced NFκB activity[J].Proceedings of the National Academy of Sciences of the United States of America,2006,103(48):18154.
[30]Kalakech H,Tamareille S,Pons S,et al.Role of hypoxia inducible factor-1αin remote limb ischemic preconditioning[J].Journal of Molecular&Cellular Cardiology,2013,65(12):98-104.
[31]Zhang J,Wang X,Vikash V,et al.ROS and ROS-Mediated Cellular Signaling[J].Oxidative Medicine&Cellular Longevity,2016,2016:5782.
[32]Letavernier E,Zafrani L,Perez J,et al.The role of calpains in myocardial remodelling and heart failure[J].Cardiovascular Research,2012,96(1):38-45.
[33]Ke J J,Yu F X,Rao Y,et al.Adenosine postconditioning protects against myocardial ischemia-reperfusion injury though modulate production of TNF-αand prevents activation of transcription factor NF-kappa B[J].Molecular Biology Reports,2011,38(1):531-538.
[34]Choi H,Kim S H,Chun Y S,et al.In vivo hyperoxic preconditioning prevents myocardial infarction by expressing bcl-2[J].Experimental Biology and Medicine,2006,231(4):463-472.
[35]Yang J,Li Y,Hu C.Ischemic preconditioning protects against myocardial,ischemia-reperfusion injury through,inhibiting toll-like receptor 4/NF-κB signaling pathway in rats[J].Journal of Central South University,2011,36(10):972.
[36]Kawano S,Kubota T,Monden Y,et al.Blockade of NFkappa B improves cardiac function and survival after myocardial infarction[J].American Journal of Physiology Heart&Circulatory Physiology,2006,291(3):1337-44.
[37]Ling H,Gray C B,Zambon A,et al.Cardiomyocytespecific p65 NF-kappa B deletion protects the injured heart by preservation of calcium handling[J].Am J Physiol Heart Circ Physiol,2013,305(7):1089-97.
[38]唐白云,刘喜利,吴钟凯,等.核转录因子-κB在体外循环术缺血预处理心肌保护机制中的作用[J].中华实验外科杂志,2007,24(2):207-208.
[39]Li T,Yu J,Chen R,et al.Mycophenolate mofetil attenuates myocardial ischemia-reperfusion injury via regulation of the TLR4/NF-B signaling pathway[J].Die Pharmazie,2014,69(11):850-5.
[40]Nishida K,Otsu K.Autophagy during cardiac remodeling[J].Journal of Molecular&Cellular Cardiology,2015,95:11-18.
[41]梁逸强,潘朝锌,何新兵,等.心室重构防治研究的进展[J].心血管康复医学杂志,2013,22(4):425-428.
[42]D'Elia N,J D Hooge.Association Between Myocardial Mechanics and Ischemic LV Remodeling[J].JACC Cardiovasc Imaging,2015,8(12):1430-43.
[43]Gordon,J W,J A.Kirshenbaum,Multiple facets of NF-kappa B in the heart:to be or not to NF-kappa B[J].Circ Res,2011,108(9):1122-32.
[44]Patel N.The effect of antisense to NF-kappa B in an albumin microsphere formulation on the progression of left-ventricular remodeling associated with chronic volume overload in rats[J].J Drug Target,2014,22(9):796-804.
[45]Frantz S.Absence of NF-kappa B subunit improves heart failure after myocardial infarction[J].FASEB J,2006,20(11):1918-20.
[46]Onai Y.Inhibition of NF-kappa B improves left ventricular remodeling and cardiac dysfunction after myocardial infarction[J].Am J Physiol Heart Circ Physiol,2007,292(1):530-8.
[47]Zelarayan L.NF-kappa B activation is required for adaptive cardiac hypertrophy[J].Cardiovasc Res,2009,84(3):416-24.
[48]Dikalov S I,Nazarewicz R R.Angiotensin Induced Production of Mitochondrial Reactive Oxygen Species:Potential Mechanisms and Relevance for Cardiovascular Disease[J].Antioxidants&Redox Signaling,2013,19(10):1085.
[49]权媛,钱民章,QUANYuan,等.胆固醇通过NADPH氧化酶诱导ROS升高,NF-κB活化进而导致内皮细胞损伤[J].中国病理生理杂志,2010,26(8):1521-1526.
[50]白玉婷,BAIYu-ting.氧化应激与心血管疾病关系的研究进展[J].医学综述,2012,18(2):192-194.
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