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Biliary Epithelial Apoptosis, Autophagy, and Senescence in Primary Biliary Cirrhosis英文文献资料.doc

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Biliary Epithelial Apoptosis, Autophagy, and Senescence in Primary Biliary Cirrhosis英文文献资料

HindawiPublishingCorporation HepatitisResearchandTreatment Volume2010,ArticleID205128,10pages doi:10.1155/2010/205128 ReviewArticle BiliaryEpithelialApoptosis,Autophagy,andSenescencein PrimaryBiliaryCirrhosis MotokoSasakiandYasuniNakanuma DepartmentofHumanPathology,KanazawaUniversityGraduateSchoolofMedicine,Kanazawa920-8640,Japan CorrespondenceshouldbeaddressedtoMotokoSasaki,m8sasaki@med.kanazawa-u.ac.jp Received28August2010;Accepted5October2010 AcademicEditor:AnnarosaFloreani Copyright?2010M.SasakiandY.Nakanuma.ThisisanopenaccessarticledistributedundertheCreativeCommonsAttribution License,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperly cited. Primarybiliarycirrhosis(PBC)isachroniccholestaticliverdiseasecharacterizedserologicallybythehighprevalenceofanti- mitochondrialautoantibodies(AMAs)andhistologicallybythecholangitisofsmallbileducts,eventuallyfollowedbyextensive lossofthesmallbileduct.Anautoimmunepathogenesisissuggestedbyclinicalandexperimentalstudies,butthereremainissues regardingtheetiology,thesigni?canceofAMAsinthepathogenesisofbileductlesions,andsoon.Theuniquepropertiesof apoptosisinbiliaryepithelialcells(BECs),inwhichthereisexposureofautoantigentothee?ectorsoftheimmunesystem,are proposedtobeacauseofbileductlesionsinPBC.Recentprogressdisclosedthatcellularsenescenceandautophagyareinvolved inbileductlesionsinPBC.SenescentBECsmaymodulatetheperiductalmicroenvironmentbyexpressingsenescence-associated secretoryphenotypes,includingvariouschemokines,andcontributetothepathogenesisofbileductlesionsinPBC. 1.Introduction and xenobiotics. The most accepted hypothesis states that PBC resultsfroman environmental insult on a genetically susceptible background. In this scenario, adaptive immu- nity, both humoral and cellular (CD4 and CD8 T cells), and innate immunity have been proposed as coplayers in immune-mediated liver damage; however, there remain many mysteries in the etiology and pathogenesis of PBC; in particula