Opportunity

NIH Reporter #5R01HL155955-05

NHLBI Research Grant: Fli1 in Myeloid Cells and Cardiac Fibrosis

Buyer

National Heart Lung and Blood Institute (NHLBI)

Posted

October 04, 2023

Respond By

July 18, 2025

Identifier

5R01HL155955-05

NAICS

541714, 541715

This opportunity involves a research grant awarded by the National Heart Lung and Blood Institute (NHLBI), part of the National Institutes of Health, to Boston University Medical Campus for investigating the role of Fli1 in myeloid cells and its contribution to cardiac fibrosis. - Government Buyer: - National Institutes of Health (NIH) - National Heart Lung and Blood Institute (NHLBI) - OEMs and Vendors: - No specific OEMs or commercial vendors are mentioned in this grant award - Products/Services Requested: - Scientific research services focused on the molecular mechanisms of Fli1 in myeloid cells - Use of genetically modified mice and patient-derived cells - Evaluation of therapeutic interventions, including Rapamycin - Unique or Notable Requirements: - Emphasis on both in vitro and in vivo studies - Focus on systemic sclerosis (SSc) and cardiac fibrosis - Integration of animal models and human samples for translational research - Investigation of disease pathways and potential therapies, not procurement of commercial products

Description

This is a research grant opportunity focused on investigating the molecular mechanisms by which the transcription factor Fli1 in myeloid cells contributes to cardiac fibrosis, particularly in the context of systemic sclerosis (SSc). The project aims to determine the molecular pathways leading to fibrosis following Fli1 depletion, assess the impact of Fli1 loss on cardiomyopathy in vivo, and explore the role of myeloid Fli1 in SSc-associated cardiomyopathy. The research involves both in vitro and in vivo studies, including the use of genetically modified mice and patient-derived cells. The goal is to understand the pathogenesis of cardiac fibrosis and evaluate potential therapeutic interventions such as Rapamycin.

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