Effect of NPHP4 deletion in a mouse model of cardio-renal syndrome
Cardio-renal syndrome (CRS), characterized by cardiac and renal dysfunction, is an increasing health problem associated with high mortality rate. Nephrocystin 4 (NPHP4) gene is the major cause of end-stage renal disease in children. We have reported NPHP4 single nucleotide polymorphism is the genetic risk for CRS and subsequent cardiovascular events in general population. However, the functional role of Nphp4 in the development of CRS has never been examined yet. To clarify the functional role of Nphp4 in the development of CRS, we generated Nphp4 knockout (KO) mice and induced CRS by performing transthoracic aortic banding (TAC).