Cardiomyocyte specific RXFP1-overexpression protects Relaxin-independently from pressure-overload induced cardiac dysfunction
Aim was to investigate the effect of cardiomyocyte-specific expression of the human Relaxin Family Peptide Receptor 1 (RXFP1) in a mouse model of pressure-overload induced cardiac dysfunction (TAC). Mice overexpressing the hRXFP1 receptor (or non-transgenic controls) underwent TAC (or Sham) surgery and were followed up for 8 weeks. Heart was removed and RNA isolated from left ventricle to perform bulk RNAseq. Overall design: Comparative gene expression profiling analysis of RNA-seq data for left ventricular tissue from hRXFP1tg mice (or non-tg controls) following 8 weeks of TAC (or Sham)  (4 group design).