[Genetic complementation studies using genetically engineered mice have revealed the impact of phospholamban on progression of cardiomyopathy].
It has been suggested that dilated cardiomyopathy and end-stage heart failure result in multiple defects in Ca(2+) cycling. By genetic ablation of a muscle specific sarcoplasmic reticulum Ca(2+) ATPase (SERCA2a) inhibitor, phospholamban, the broad phenotypes of murine model of dilated cardiomyopathy could be almost completely rescued. Thus, phospholamban inactivation or disruption of interaction between phospholamban and SERCA2a may provide a novel therapeutic approach for preventing the progression of heart failure.
Minamisawa
S
S
Department of Pediatric Cardiology, The Heart Institute of Japan, Tokyo Women's Medical University.