Grant: Project Grant

It has been well established that the adult female heart has an inherently greater resistance to damage after a reduction of blood flow. Despite these findings, the underlying events providing the female heart greater protections remains equivocal. In addition, it also remains unknown if the protective trait of the female heart can be unmasked in the adult male heart. Work from my lab has reported that an immunosuppressant drug known as rapamycin led to a significant expansion of the scar following administration to the adult female rat heart after the experimental induction of a heart attack. These data have led to the premise that the target of rapamycin a protein denoted mTOR may provide the female heart greater resistance to damage. Therefore, the present grant proposal will attempt to identify the signaling events that regulate mTOR activity, and elucidate that targets of mTOR that provide the female heart greater resistance to damage after a heart attack.