Project description:The purpose of the experiment is to assess the genes expression changes in the heart in response to transverse aortic constriction (TAC)-induced pressure overload, and to identify the genes which are involved in the pathogenesis of heart failure induced by hypertension; thereafter examining the individual gene function in the heart and discovering the novel drug targets to prevent heart failure. Wild-type C57 mice were subjected to transverse aortic constriction (TAC) for 12 weeks (sham as the control, Con). The hearts were collected and snap frozen for the following experiments.

2023-05-23 | E-MTAB-12979 | biostudies-arrayexpress

Heart Failure with Preserved Ejection Fraction - Mouse Heart and Lung Tissue & Comorbidities

Project description:FASILOX analysis of heart and lung tissue form mice with heart failure with preserved ejection fraction and several comorbidities.

2024-10-02 | PXD056447 | JPOST Repository

mRNA sequencing of mouse and human heart tissue

Project description:mRNA sequencing of mouse and human heart tissue

| PRJNA549848 | ENA

ARRDC4 knock out Mouse Heart Analysis

Project description:ARRDC4 knock out Mouse Heart Analysis

| PRJNA773414 | ENA

Transcriptome analysis of aging mouse heart compared with adult heart

Project description:Transcriptome analysis of aging mouse heart compared with adult heart

| PRJNA835808 | ENA

Mouse Heart Immunoprecipitation MS

Project description:Screened coimmunoprecipitates of endogenous HSC70 in the mouse heart tissue using mass spectrometry under unstressed condition

2023-06-06 | PXD042742 | JPOST Repository

Transcriptomic analysis of DSG2-W2A mouse heart tissue

Project description:Transcriptomic analysis of DSG2-W2A mouse heart tissue. In DSG2-W2A mice, adhesion of the desmosomal molecule desmoglein-2 (DSG2) is abrogated via mutation of its’ major interaction mechanism (so-called "tryptophan swap" (Harrison, Brasch et al. 2016)). Adult DSG2-W2A mut/mut mice resemble the phenotype of Arrhythmogenic Cardiomyopathy (ACM or ARVC) with biventricular fibrosis, impaired systolic output function and arrhythmia. This phenotype was present in mutant mice analysed at the age of 9 weeks compared to 5-days old hearts, which showed no morphological alterations.

2022-12-05 | GSE181868 | GEO

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