Mouse Phosphodiesterase 1C, Calmodulin Dependent (PDE1C) ELISA Kit-Sandwich

PDE1C is abundantly expressed in the mouse heart and influences cardiac function by regulating the cAMP signaling pathway. Research has identified PDE1C as a crucial regulator in cardiac remodeling and dysfunction. In models of pressure overload-induced myocardial hypertrophy and fibrosis, the absence or inhibition of PDE1C significantly reduces pathological changes such as cardiomyocyte apoptosis, fibrosis, and ventricular remodeling. Additionally, PDE1C modulates cardiomyocyte survival and apoptosis via the cAMP/PKA and PI3K/AKT signaling pathways. Consequently, PDE1C is vital for cardioprotection, and its inhibition could be a potential strategy for treating heart failure. Moreover, PDE1C is expressed in the mouse brain, where it is involved in neuronal migration and development.