ArrayExpress Uploader06288failing, atherosclerosisapoE-deficientfailing, atherosclerosisapoE-deficientcontrolwild typecontrolwild typeatherosclerosisapoE-deficientatherosclerosisapoE-deficientarrayexpress_sid6Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We used 18 month-old apolipoprotein E...E-GEOD-25767/profile/8773/arrayexpressuploader26atherosclerosisheartDec.12, 2014Falsecardiac-gene-expression-profiling-of-apoe-deficienE-GEOD-25767_A-AFFY-45Cardiac gene expression profiling of apoE-deficient mice receiving heart failure treatment with the anti-ischemic drug ranolazineNov.11, 2014Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We used 18 month-old apolipoprotein E (apoE)- deficient mice as a model of atherosclerosis-induced heart failure to analyze whether the anti-ischemic drug ranolazine could retard the progression of heart failure. The study showed that 2 months of ranolazine treatment improved cardiac function of 18 month-old apoE-deficient mice with symptoms of heart failure as assessed by echocardiography. To identify changes in cardiac gene expression induced by treatment with ranolazine a microarray study was performed with heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts. The microarray approach identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine. Microarray gene expression profiling was performed with heart tissue isolated from (i) untreated 18 month-old apoE-deficient mice with heart failure relative to (ii) 18 month-old apoE-deficient mice treated for two months with the anti-ischemic drug ranolazine (200 mg/kg), and (iii) age-matched non-transgenic C57BL/6J (B6) control mice.http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-25767mousehttp://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-25767/samples/