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NLRP3与心血管疾病关联的研究进展
作者:郭志浩  王莉娜  马根山 
单位:东南大学附属中大医院 心血管内科, 江苏 南京 210009
关键词:NLRP3 心血管疾病 治疗策略 文献综述 
分类号:R541.4
出版年·卷·期(页码):2014·33·第一期(103-107)
摘要:

炎症小体是属于模式识别受体家族的多聚体蛋白,主要包括NLRPs、NLRC、NAIP和AIM2。其中,NLRP3参与冠状动脉粥样硬化、心肌梗死、缺血/再灌注损伤以及心肌梗死后心脏重构等心血管疾病的病理生理过程,影响临床结局。有效调控NLRP3有助于预防、治疗心血管疾病。本文对NLRP3与心血管疾病关联的研究进展作一综述,并讨论心血管疾病潜在的抗炎症治疗策略。

参考文献:

[1] GARG N J.Inflammasomes in cardiovascular diseases[J].Am J Cardiovasc Dis, 2011, 1(3):244-254.
[2] DUEWELL P, KONO H, RAYNER K J, et al.NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals[J].Nature, 2010, 464(7293):1357-1361.
[3] ZHOU R, TARDIVEL A, THORENS B, et al.Thioredoxin-interacting protein links oxidative stress to inflammasome activation[J].Nat Immunol, 2010, 11(2):136-140.
[4] STOKES L, JIANG L H, ALCARAZ L, et al.Characterization of a selective and potent antagonist of human P2X(7) receptors, AZ11645373[J].Br J Pharmacol, 2006, 149(7):880-887.
[5] LAMKANFI M, DIXIT V M.Inflammasomes and Their roles in disease and healthy[J].Annu Rev Cell Dev Biol, 2012, 28:137-161.
[6] MASTERS S L, LATZ E, O'NEILL L A.The inflammasomes in atherosclerosis and type 2 diabetes[J].Sci Transl Med, 2011, 3(81):81ps17.
[7] LINDEMANN S, TOLLEY N D, DIXON D A, et al.Activated platelets mediate inflammatory signaling by regulated interleukin 1-beta synthesis[J].J Cell Biol, 2001, 154(3):485-490.
[8] de NOOIJER R, von der THVSEN J H, VERKLEIJ C J, et al.Overexpression of IL-18 decreases intimal collagen content and promotes a vulnerable plaque phenotype in apolipoprotein-E-deficient mice[J].Arterioscler Thromb Vasc Biol, 2004, 24(12):2313-2319.
[9] LYER S S, PULSKENS W P, SADLER J J, et al.Necrotic cells trigger a sterile inflammatory response through the Nlrp3 inflammasome[J].Proc Natl Acad Sci USA, 2009, 106(48):20388-20393.
[10] YAMAMOTO M, YAGINUMA K, TSUTSUI H, et al.ASC is essential for LPS-induced activation of procaspase-1 independently of TLR-associated signal adaptor molecules[J].Genes Cells, 2004, 9(11):1055-1067.
[11] TAKAHASHI M.Role of the Inflammasome in Myocardial Infarction[J].Trends Cardiovasc Med, 2011, 21(2):37-41.
[12] KAWAGUCHI M, TAKAHASHI M, HATA T, et al.Inflammasome activation of cardiac fibroblasts is essential for myocardial ischemia/reperfusion injury[J].Circulation, 2011, 123(6):594-604.
[13] McDONALD B, PITTMAN K, MENEZES G B, et al.Intravascular danger signals guide neutrophils to sites of sterile inflammation[J].Science, 2010, 330(6002):362-366.
[14] ARTLETT C M.The role of the NLRP3 inflammasome in fibrosis[J].Open Rheumatol J, 2012, 6:80-86.
[15] FIX C, BINGHAM K, CARVER W, et al.Effects of interleukin-18 on cardiac fibroblast function and gene expression[J].Cytokine, 2011, 53(1):19-28.
[16] PLATIS A, YU Q, MOORE D, et al.The effect of daily administration of IL-18 on cardiac structure and function[J].Perfusion, 2008, 23(4):237-242.
[17] MEZZAROMA E, TOLDO S, FARKAS D, et al.The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse[J].PNAS, 2011, 108(49):19725-19730.
[18] NATHAN A B, PAUL L B, DANIEL A M, et al.The Nlrp3 inflammasome promotes myocardial dysfunction in structural cardiomyopathy through interleukin-1β[J].Exp Physiol, 2013, 98(2):462-472.
[19] ABBATE A, KONTOS M C, GRIZZARD J D, et al.Interleukin-1 blockade with anakinra to prevent adverse cardiac remodeling after acute myocardial infarction(Virginia Commonwealth University Anakinra Remodeling Trial[VCU-ART] Pilot Study)[J].Am J Cardiol, 2010, 105(10):1371-1377.
[20] WHELAN R S, KAPLINSKIY V, KITSIS R N.Cell death in the pathogenesis of heart disease:mechanisms and significance[J].Annu Rev Physiol, 2010, 72:19-44.
[21] HERMANSSON C, LUNDQVIST A, WASSLAVIK C, et al.Reduced expression of NLRP3 and MEFV in human ischemic heart tissue[J].Biochem Biophys Res Commun, 2013, 430(1):425-428.
[22] PELEGRIN P, SURPRENANT A.Dynamics of macrophage polarization reveal new mechanism to inhibit IL-1beta release through pyrophosphates[J].EMBO J, 2009, 28(14):2114-2127.
[23] WILHELM K, GANESAN J, MULLER T, et al.Graft-versus-host disease is enhanced by extracellular ATP activating P2X7R[J].Nat Med, 2010, 16 (12):1434-8.
[24] ARULKUMARAN N, UNWIN R J, TAM F W.A potential therapeutic role for P2X7 receptor (P2X7R) antagonists in the treatment of inflammatory diseases[J].Expert Opin Investig Drugs, 2011, 20(7):897-915.
[25] MA W, HUI H, PELEGRIN P, et al.Pharmacological characterization of pannexin-1 currents expressed in mammalian cells[J].J Pharmacol Exp Ther, 2009, 328(2):409-418.
[26] MOLTO A, OLIVE A.Anti-IL-1 molecules:new comers and new indications[J].Joint Bone Spine, 2010, 77(2):102-107.
[27] LOPEZ-CASTEJON G, PELEGRIN P.Current status of inflammasome blockers as anti-inflammatory drugs[J].Expert Opin Investig Drugs, 2012, 21(7):995-1007.
[28] DUNCAN J A, BERGSTRALH D T, WANG Y, et al.Cryopy-rin/NALP3 binds ATP/dATP, is an ATPase, and requires ATP binding to mediate inflammatory signaling[J].Proc Natl Acad Sci USA, 2007, 104(19):8041-8046.
[29] COLL R C, O'NEILL L A.The cytokine release inhibitory drug CRID3 targets ASC oligomerisation in the NLRP3 and AIM2 inflammasomes[J].PLoS One, 2011, 6(12):e29539.
[30] THACKER J D, BALIN B J, APPELT D M, et al.NLRP3 inflammasome is a target for development of broad-spectrum anti-infective drugs[J].Antimicrob Agents Chemother, 2012, 56(4):1921-1930.

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