# Fatty acid-binding proteins sustain endothelial glycolysis and arterial programming in pulmonary arterial hypertension

> **NIH NIH R01** · UNIVERSITY OF ARIZONA · 2023 · $575,845

## Abstract

Title: Fatty acid-binding proteins sustain endothelial glycolysis and arterial programming in
 pulmonary arterial hypertension
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 vascular remodeling and obliterative
vascular lesion formation remain unclear. Fatty acid metabolism dysfunction is linked to PAH. However,
the mechanistic role of fatty acid metabolism in regulating pulmonary vascular remodeling in the
pathogenesis of PAH has not been reported. We hypothesize that endothelial fatty acid-binding proteins
4 and 5 (FABP4-5) regulate endothelial glycolysis and arterial programming through HIF-2a/SOX17
signaling which contributes to severe vascular remodeling in the pathogenesis of PAH. We will 1) define
the novel role of endothelial FABP4-5 in the pathogenesis of PAH using multiple transgenic animal
models. 2) delineate the cellular and molecular mechanisms that FABP4-5 induces arterial programming
and 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:** 10657101
- **Project number:** 1R01HL162794-01A1
- **Recipient organization:** UNIVERSITY OF ARIZONA
- **Principal Investigator:** Zhiyu Dai
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $575,845
- **Award type:** 1
- **Project period:** 2023-04-15 → 2027-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10657101

## Citation

> US National Institutes of Health, RePORTER application 10657101, Fatty acid-binding proteins sustain endothelial glycolysis and arterial programming in pulmonary arterial hypertension (1R01HL162794-01A1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10657101. Licensed CC0.

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