Early cardiac dysfunction is rescued by upregulation of <scp>SERCA</scp>2a pump activity in a rat model of metabolic syndrome

Abstract

In early stage, metabolic syndrome primarily disturbs SERCA2a function in the heart, but consequential haemodynamic dysfunction is prevented by upregulation of SERCA2a protein level and phosphorylation pathways regulating PLB. However, this compensated state is very vulnerable to a further decline in SERCA2a function.