Project Details
Description
Project Summary
Pulmonary arterial hypertension (PAH) is a lethal disease with a median survival of only 5-7 years.
Pathophysiologically, PAH is a progressive vasculopathy of the precapillary pulmonary vessels that increases
pulmonary arterial pressures and pulmonary vascular resistance while reducing pulmonary arterial compliance.
The changes in the pulmonary vasculature augment the work load of the right ventricle, which ultimately results
in right ventricular dysfunction (RVD). The presence of RVD is the greatest risk factor for death in PAH;
however, no current PAH therapies actually target the RV directly. In this proposal, we will investigate the
hypothesis that GP130 activation in RV cardiomyocytes promotes cardiomyocyte dysfunction via microtubule
remodeling which causes t-tubule derangements and mitochondrial metabolic dysfunction. We will use state-
of-the-art approaches to probe the molecular and physiological effects of GP130 antagonism on right
ventricular function in porcine RV failure.
Status | Active |
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Effective start/end date | 5/1/22 → 4/30/24 |
Funding
- National Heart, Lung, and Blood Institute: $675,355.00
- National Heart, Lung, and Blood Institute: $675,355.00
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