Downregulation of the Na ⁺ -Creatine Cotransporter in Failing Human Myocardium and in Experimental Heart Failure

Abstract

Both in human and in experimental heart failure, creatine transporter protein content is reduced. This mechanism may contribute to the depletion of creatine compounds and thus to the reduced energy reserve in failing myocardium. This finding may have therapeutic implications, suggesting a search for treatment strategies targeted toward creatine transport.