# General Capillary to Arterial Endothelial Cell Transition in Pulmonary ArterialHypertension

> **NIH NIH R01** · WASHINGTON UNIVERSITY · 2024 · $715,847

## Abstract

Project Summary
 Pulmonary arterial hypertension (PAH) is characterized by a progressive increase of pulmonary
vascular resistance and obliterative pulmonary vascular remodeling that result in right heart hypertrophy,
failure, and premature death. The underlying mechanisms of loss of capillary endothelial cells (ECs) and
obliterative vascular lesion formation remain unclear. Our preliminary data showed that arterial
programing was evident in human PAH patients and rodents. We hypothesize that general capillary ECs
program to arterial ECs through HIF-2α-Cdk19/Sox17/Notch4 signaling which contributes to the
pathogenesis of PAH. Completing our proposed study will provide a novel therapeutic strategy for the
effective treatment of PAH in patients.

## Key facts

- **NIH application ID:** 11175168
- **Project number:** 7R01HL170096-02
- **Recipient organization:** WASHINGTON UNIVERSITY
- **Principal Investigator:** Zhiyu Dai
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $715,847
- **Award type:** 7
- **Project period:** 2023-09-15 → 2027-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11175168

## Citation

> US National Institutes of Health, RePORTER application 11175168, General Capillary to Arterial Endothelial Cell Transition in Pulmonary ArterialHypertension (7R01HL170096-02). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/11175168. Licensed CC0.

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