摘要
RecentstudiesrevealingtheimportantrolesofmicroRNAs（miRNAs）inregulatingexpressionofionchannelgeneshaveopeneduparesearchfieldforextendinganddeepeningourinvesti-gationintothecardiacexcitabilityandtheassociatedarrhythmogenesis.Cardiacexcitability,thefundamentalpropertyofthecardiacmyocytes,definesthecardiacconduction,repolarization,automaticity,intracellularcalciumhandling,andtheirregionalheterogeneity.OurpreviousandongoingstudiesandtheworkfromotherlaboratorieshavedemonstratedthesignificantinvolvementofmiRNAsinregulatingeveryaspectsofcardiacexcitability.Wehavefoundearlierthatthemuscle-specificmiRNAmiR-1boostsupthearrhythmogenicpotentialthroughtargetinggapjunctionchannelconnexin43inmyocardialinfarction.AsubsequentstudyrevealedthatmiR-1canalsocausearrhythmiasbyimpairingCa2+handlingbytargetingphosphatase.Wethenidentifiedanothermuscle-specificmiRNAmiR-133promotesabnormalQTprolongationbyrepressingHERGK+channelexpressionindiabeticcardiomyopathy.Subsequently,wediscoveredthatbothmiR-1andmiR-133areinvolvedinthereexpressionofpacemakerchannelsHCN2/HCN4toenhanceabnormalautomaticityincardiachypertrophy.Recently,wefurtheridentifiedmiR-328asanimportantdeterminantforatrialfibrillation（AF）andtheassociatedadverseatrialelectricalremodelingviatargetingL-typeCa2+channels.Whilealltheabove-mentionedmiRNAsareproarrhythmic,wehavenewlyidentifiedforthefirsttimeanaturalantiarrhythmicmiRNAmiR-26.WefoundthatallthreemembersofthemiR-26familyisdownregulatedintheirexpressioninAFtissuesandthisdownregulationincreasesAFvulnerabilityasaresultofremovalofanendogenousantiarrhythmicfactor.miR-26downregulationshortensatrialactionpotentialfavoringAFbyincreasinginwardrectifierK+current（IK1）density.ThisiscausedbyanupregulationofKir2.1K+channelsu
出版日期
2011年05月21日（中国期刊网平台首次上网日期，不代表论文的发表时间）
