Project Details
Description
Project Summary
The goals of this project are to train Kurt Prins MD, PhD as a physician-scientist in Cardiology and advance the
understanding of right ventricular dysfunction in pulmonary arterial hypertension (PAH). Dr. Prins is currently a third
year Cardiology fellow in the Physician-Scientist Training Program, a combined research and clinical track dedicated to
training the next generation of physician-scientist at the University of Minnesota. Dr. Prins has elected to conduct his
research training in the laboratory of Dr. Joseph Metzger, a leader in molecular cardiac physiology who has a long track
record of obtaining NIH funding and experience training physician-scientists. Dr. Prins has chosen two experts in
pulmonary arterial hypertension research: Drs. Stephen Archer and E. Kenneth Weir to be on his mentoring committee to
further guide him in his early career. Dr. Prins’ educational objectives include gaining expertise in cardiac physiology by
working in a lab of an established investigator in cardiology and collaborating with an expert in PAH, attending seminars
to gain further exposure to outside investigators and build collaborations, and taking courses to prepare for future grant
applications. The research project will investigate two distinct mechanisms of junctophilin-2 misregulation that contribute
to right ventricular dysfunction in PAH. Dr. Prins authored a manuscript that showed increased microtubule density was
associated with junctophilin-2 misregulation resulting in t-tubule disruptions and calcium mishandling in Duchenne
cardiomyopathy. Now he will define the role of junctophilin-2 in RV dysfunction in PAH, a disease that he has worked to
specialize in clinically. Thus, this proposed training period will allow Dr. Prins to combine his basic science and clinical
interests by studying the link between junctophilin-2 misregulation due to improper trafficking on a pathologically
remodeled microtubule cytoskeleton and miR-24-mediated repression and RV dysfunction in PAH. The project will
determine if misregulation of junctophilin-2 leads to altered t-tubule structure, calcium mishandling, and ultimately RV
dysfunction in pulmonary arterial hypertension. Also, it will also test the hypothesis that normalizing junctophilin-2 with
colchicine treatment and by inhibiting miR-24 could be novel therapeutic strategies to improve RV function in PAH.
Status | Finished |
---|---|
Effective start/end date | 7/1/18 → 6/30/23 |
Funding
- National Heart, Lung, and Blood Institute: $171,396.00
- National Heart, Lung, and Blood Institute: $171,396.00
- National Heart, Lung, and Blood Institute: $123,263.00
- National Heart, Lung, and Blood Institute: $171,396.00
- National Heart, Lung, and Blood Institute: $171,396.00
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