粘着斑激酶在肺纤维化的发病机制研究进展
摘要
<正>纤维化是一种难治性的疾病,它以成纤维细胞增生和过多的细胞外基质蛋白(ECM)沉积为主要特征,可发生在机体的各器官组织。肺纤维化(PF)疾病演变的过程,即由炎症介质及细胞浸润于下呼吸道为起始阶段,同时伴有多种促纤维化因子、肌成纤维细胞(MF)等的释放,可引起血管内皮细胞以及肺泡上皮细胞受损,致细胞外基质蛋白和胶原沉积,最终引起肺组织结构的异常重塑,呼吸衰竭而死亡。粘着斑激酶(FAK)在其发生和发展中起到了举足轻重的作用。本文
引文
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[24]Klossner S,Li R,Ruoss S,Durieux AC,et al.Quantitative changesin focal adhesion kinase and its inhibitor,FRNK,drive loaddependent expression ofcostamere components[J].Am J Physiol Regul Integr Comp Physiol,2013,305(6):R647-657.
[25]Schneider M.,Kostin S,Claes C,et al.S100A4is regulated in injured myocardium and promotes growth and survival of cardiac myocytes[J].Cardiovasc Res,2007,75(1):40.
[2]Hildebrand J D,Taylor J M,Parsons J T.An SH3domaincontaining GTPase-activating protein for Rho and Cdc42associates with focal adhesion kinase[J].Mol cell Biol,1996,16(6):3169-3178.
[3]Fumto Y,Ilic D,Kanazawa S,et a1.Mesodemal defect in late phase of gastrulation by a targeted mutation of focal adhesion kinase,FAK[J].0ncogene,1995,11(10):1989-1995.
[4]Su JM,Gui L,zhou YP,et a1.Expression of focal adhesion kinase and alpha5and betal integrins in carcinomas and its clinical significance[J].world J Gastroenterol,2002,8(4):613-618.
[5]陈尧,李瑞祥,刘执玉.人直肠腺癌血管内皮细胞局部粘附激活酶的表达[J].解剖学杂志,2000,23(6):533-535.
[6]Hassid A,Huang SL,Yan J.Role of PTP-1Bin aortic smooth msucle cell motility and tyrosine phosphorylation of focal adhesion proteins[J].Am J Physiol,1999,277(46):H 192-H 199.
[7]Duhen T,Geiger R,Jarrossay D,et al.Production of interleukin22but not interleukin 17by a subset of human skin-homing memory T cells,Nat immnol,2009,10(56):857-863.
[8]Manel N,Unutmaz D,Littman DR,The differentiation of human T(H)-17cells requires transforming growth factor-beta and induction of the nuclear receptor RORgammat.Nat Immunol,2008,9(6):641-649.
[9]Cospedal R,Abedi H,Zachary I.Platelet-dervied growth factorBB(PDGF-BB)regulation of migration and focal adhesion kinase phosphorylation in rabbit aortic vascular smooth muscle cells:roles of phosphatidylinositol 3-kinase and mitogen-acti-vated protein kinases.Cardiovasc Res,1999,41:708-721.
[10]Brown Mc,Cary LA,Jamieson JS,et a1.src and FAK kinases cooperate to phosphorylate pKL,stimulate its focal adhesion localization,and regulate cell spreading and protrusiveness.Mol Biol Cell,2005,16:4316-4328.
[11]Jurek A,Heldin CH,Lennartsson J.Platelet-derived growth factor-induced signaling pathways interconnect to regulate the temporal pattern of Erk1/2phosphorylation[J].Cell Signal,2011,23(1):280-287.
[12]Taylor JM,Mack CP,Nolan K,Regan CP,Owens GK,Parsons T.Selective expression of an endogenous inhibitor of FAK regulates proliferation and migration of vascular smooth muscle cells.Mol Cell Biol 2001;21(5):1565-1572.
[13]HEHLGANS S,HAASE M,CORDES N.signalling via integrins:implications for cell survival and anticancer strategies[J].Biochim Biophys Acta,2007,1775:163-180.
[14]Schaller MD,Borgman CA,Parsons JT:Autonomous expression of a noncatalytic domain of the focal adhesion-associated protein tyrosine kinase pp125FAK.Mol Cell Biol 1993,13:785e791.
[15]Taylor JM,Mack CP,Nolan K,Regan CP,Owens GK,Parsons JT:Selective expression of an endogenous inhibitor of FAK regulates proliferation and migration of vascular smooth muscle cells.Mol Cell Biol 2001,21:1565e1572.
[16]Hauck CR,Hsia DA,Puente XS,Cheresh DA,Schlaepfer DD:FRNK blocks v-Src-stimulated invasion and experimental metastases without effects on cell motility or growth.EMBO J 2002,21:6289e6302.
[17]ReifZ,LangA.The role of focal adhesion kinase phosphatidylinositol-3-kinase-Akt signaling in hepatic stellate cell proliferation and typeⅠcollagen expression[J].Biol Chem,2003,278(10):8083-8090.
[18]Heidkamp MC,Bayer AL,Kalina JA,et a1.Adhesions and Induces Anoikis in Neonatal Rat Ventricular Myocytes.Circ Res,2002,90(1 2):1282-1 289.
[19]Wolf BB,Schuler M,Echeverri F,et a1.Caspase-3is the Primay Activator of Apoptotic DNA Fragmentation Via DNAFragmentation Factor 45/Inhibitor of Caspase-activated DNase Inactivation.J Biol Chem,1 999,274(43):30651-30656.
[20]Chapman HA:Disorders of lung matrix remodeling.J Clin Invest 2004,113:148e157.
[21]Desmouliere A,Darby I,Gabbiani G:Normal and pathologic softtissue remodeling:role of the myofibroblast,with special emphasis on liver and kidney fibrosis.Lab Invest 2003,83:1689e1707.
[22]Jenkins RG,Su X,Su G,Scotton CJ,Camerer E,Laurent GJ,Davis GE,Chambers RC,Matthay MA,Sheppard D:Ligation ofprotease-activated receptor 1enhances alpha(v)beta6integrindependent TGF-beta activation and promotes acute lung injury.J Clin Invest 2006,116:1606e1614.
[23]Liu X,Hu H,Yin JQ:Therapeutic strategies against TGF-beta signaling pathway in hepatic fibrosis.Liver Int 2006,26:8e22.
[24]Klossner S,Li R,Ruoss S,Durieux AC,et al.Quantitative changesin focal adhesion kinase and its inhibitor,FRNK,drive loaddependent expression ofcostamere components[J].Am J Physiol Regul Integr Comp Physiol,2013,305(6):R647-657.
[25]Schneider M.,Kostin S,Claes C,et al.S100A4is regulated in injured myocardium and promotes growth and survival of cardiac myocytes[J].Cardiovasc Res,2007,75(1):40.