心衰中的分子医学系列英文.pptxVIP

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心衰中的分子医学系列英文.pptx

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Series on Molecular Medicine in Heart FailureIon Channel Remodeling in Heart Failure王擎(Qing K. Wang)Professor and DeanCollege of Life Science and TechnologyHuazhong University of Science and TechnologyAndProfessor, Director, StaffCenter for Cardiovascular GeneticsCleveland Clinic Lerner College of Medicine of Case Western Reserve University and Cleveland Clinic Cleveland, Ohio, USA Ion Channel Remodeling and Heart FailureHeart failure is a major cause of sudden deathAbout 50% of heart failure deaths are due to ventricular tachycardia (VT)Prolongation of the action potential duration is a consistent finding in heart failure(A) Schematic cardiac action potential (AP) with phases and principal corresponding ion currents indicatedMichael, G. et al. Cardiovasc Res 2009 81:491-499; doi:10.1093/cvr/cvn266NTG cellCa-mediated excitation-contraction couplingCa-ChRyR2SRNa-ChSERCAVENTRICULARMYOCYTENa/CaexchangerA schematic diagram showing the changes in Ca2+ handling and contractility and the potential compensatory function of ion-channel remodelling that causes action potential (AP) duration (APD) prolongation in congestive heart failureMichael, G. et al. Cardiovasc Res 2009 81:491-499; doi:10.1093/cvr/cvn266Copyright restrictions may apply.Cardiac Sodium Channel Nav1.5 and Heart FailureEncoded by SCN5A geneOn chromosome 3p21220 kDaHighly expressed in heartGenerate and propagate APoutphase 1inCardiac Sodium ChannelCardiac Action PotentialIIIIIIIVN1325SGain-of-Function Mutations in SCN5A Cause Long QT Syndrome (LQTS)N1325SIncomplete channel inactivationCLOSEDOPENINACTIVEIncreased APDProlonged QTcVTSudden DeathLate INaN1325SGeneration of Transgenic TG-WT and TG-LQT3 Mice1. TG-LQT3 (MTG): generated by transgenic overexpression of mutant SCN5A mutation N1325S in the mouse heart2. TG-WT (WTG): generated by transgenic overexpression of wild type SCN5A in the mouse heart Not1BstEIIBstEIINot1Probe AProbe BN1325Sa-mMHCphGH plATG-LQT3 (SCN5A)Southern blota-mMHCphGH plATG-WT (SCN5A)Wes