Research Report 2010 - MDC

Graduate StudentsPhilipp DuBoisSanthosh Kumar GhadgeJida HamatiLydia HeringDörte LodkaClaudia NoackMarcel NowakAnke RengerBastian SpallekAnnett SpitzlTimm ZörgiebelTechnical AssistantsMarlies DudaMarlies GriebenRené KolbBeatrice LeipAnika LindnerJutta MeiselJeanette MothesBärbel PohlTanja SchalowAstrid SchicheFigure 1. αMHC-dependent β-catenin depletion attenuates post-infarctLV remodeling. β-catenin depletion (β-cat ∆ex3–6 ) results in improved fractionalshortening 4 weeks after infarct associated with a prominentsub-endocardial and sub-epicardial layer of cardiomyocytes as identifiedby Troponin T (cTnT) staining.and his colleagues provide evidence that α1-autoantibodiesare of potential pathophysiological relevanceand could represent a factor contributing to the developmentof refractory hypertension.Experimental Electrophysiology in Heart FailureRobert FischerIn endstage heart failure a significant portion of heartfailure patients die suddenly due to malignant arrhythmias.Robert Fischer and his subgroup are performingelectrophysiological examinations in murine models toevaluate the risk of sustained ventricular arrhythmias.Recently, they were able to substantiate the beneficialeffects of omega-3-polyunsaturated fatty acids in preventingarrhythmias in a heart failure model.Patent Application 01/2009: EP18174 “Novel eicosanoidderivatives”.Genetics of Hypertrophy and Heart FailureCemil Özcelik, Christian Geier, Andreas Perrot,Maximilian PoschHypertrophic cardiomyopathy (HCM) is the most commongenetic myocardial disease with a prevalence of0.2 % in adults. Left ventricular hypertrophy in theabsence of other causes is the clinical hallmark. In addition,the clinical phenotype is characterized by suddencardiac death. Mutations in a number of sarcomericcontractile-protein genes are causative in approximately60 % of individuals with HCM. Christian Geier fromCemil Özcelik´s subgroup has identified a missenseCardiovascular and Metabolic Disease Research 39