Paul H Goldspink, PhD
Research Associate Professor
Department of Physiology and Biophysics
Contact
Building & Room:
COMRB 2097
Office Phone:
Fax:
Lab
Building & Room:
COMRB 2088
Email:
Related Sites:
Interests Heading link
Molecular mechanisms and signaling events mediating the pathogenesis of cardiovascular disease.
About
My research is directed to the study of pathophysiologic determinants of cardiovascular disease, as well as promoting physiologic and restorative adaptation. This work primarily focuses on the role of cell-cell mechanical, neurohormonal and growth factor signaling to study integrated cardiovascular physiology, and cellular signaling events associated with dysregulation of homeostatic mechanisms within the heart. Ongoing collaborative projects aim to elucidate the mechanisms by which defective biochemical and mechanical signals initiated in the endothelium and cardiac myocyte components of the heart, cross-talk, and contribute to heart failure disease progression. In the context of physiologic adaption, we have been investigating the function of an IGF-1 isoform (Mechano-growth factor (MGF)), since it is expressed in response to myocardial ischemia and hemodynamic stress in young hearts, but not the aging heart. We aim to understand the function of MGF’s unique extension peptide (or E-domain) and its interactions with 14-3-3 proteins to determine whether modulation intracellular signaling pathways is sufficient to restore contractile function during heart failure and in the aging heart. These studies integrate use of molecular, biochemical and cellular based technologies and discovery platforms in model organisms, to inform us of how changes in cellular physiology manifest and alter the normal state of organ and systems physiology.