Functional role of IP3 receptors in the regulation of cardiac myofibroblasts

Cardiovascular disorders remain the number one cause of mortality in United States, with ischemic cardiac disease as the major sequela underlying such lethality. This is the first investigation into the functional role of intracellular calcium fluxes in cardiac fibroblasts using a specific and novel animal model in which all isoforms of a main calcium channel are deleted. Our studies, relevant to public health and to the NIH mission to discover basic mechanisms underlying human disease, suggest an unprecedented role for intracellular calcium release channels in the pathophysiology of cardiac fibrosis following myocardial infarction via pathways that involve the activation and persistence of myofibroblasts after ischemic injury.