Transcriptome profiling of DDAH1 systemic knockout in a mouse model of HFpEF

Dimethylarginine dimethylaminohydrolase 1 (DDAH1) is a key enzyme regulating nitric oxide synthesis. Its role in heart failure with preserved ejection fraction (HFpEF), a complex clinical syndrome with limited therapeutic options, remains unclear. This study aims to delineate the global transcriptomic alterations mediated by systemic DDAH1 deficiency in the context of HFpEF, thereby identifying potential pathways and therapeutic targets.We performed RNA sequencing (RNA-seq) on heart tissue samples from a well-characterized mouse model of HFpEF. The experimental design comprises four distinct groups to allow for comparative analysis:Wild-type control (WT_ctrl) Wild-type HFpEF (WT_hfpef) Systemic DDAH1 knockout control (DDAH1-KO_ctrl)Systemic DDAH1 knockout HFpEF (DDAH1-KO_hfpef)