Award Summary

One grant available.
$40,000 a year for two years.
Target audience: Junior investigators interested in pulmonary arterial hypertension (PAH) research.

This research grant supports the careers of junior investigators interested in PAH research. Each year, PHA grants one award to a promising researcher likely to make a strong, sustained impact in PAH research.

Proposals should examine the pathophysiology of PAH to clarify mechanistic pathways and identify new therapeutic targets or biomarkers in adult or pediatric pulmonary hypertension. The project potentially should apply to human pulmonary vascular diseases.

Applicants may request up to $40,000 a year for two years. The funds can cover salaries and/or supplies. Indirect costs won’t be paid to sponsoring institutions.

PHA encourages investigators to connect through its professional network, PH Clinicians and Researchers, during their research.

Apply by 5 p.m. ET, March 15 2022. Review the policies and guidelines for eligibility and submission instructions.

Sponsorship support provided by Janssen Pharmaceuticals Inc. through a partnership with PHA.

Questions? Contact us.

Current Grant Awardee

Vineet Agrawal, M.D.

“TGF-beta Receptor 3 as a Novel Mediator of Endothelial Metabolism in PAH”
Term: December 2020 – December 2022
Instructor, Division of Cardiovascular Medicine
Vanderbilt University Medical Center (VUMC)

Pulmonary arterial hypertension (PAH) is a rare but life threatening disease in which arteries of the lung progressively get clogged and ultimately cause failure of the heart due to clogged lung arteries. There are therapies that have improved the lives of patients with PAH by reducing the stress on the heart, but no therapies to date are actually capable of reversing the clogged lung arteries that occur in PAH. This is because we don’t completely understand why lung arteries get clogged, and thus don’t understand how best to fix the problem. This proposal aims to learn about a new signal, TGF beta receptor 3, that may be important in learning why lung arteries get clogged in PAH. Specifically, we believe that changes in how the lung arteries use energy/fuel from nutrients in the body is important in driving the processes that ultimately lead to clogging of the arteries. We also believe that TGF beta receptor 3 not only plays a role in altering energy metabolism of the lung arteries, but can also be targeted to improve energy metabolism and reverse changes in the lung arteries. This proposal will directly study TGF beta receptor 3’s role in PAH and identify whether targeting it by increasing its levels can reverse lung artery clogging in PAH.