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Multi-omic profiling of pulmonary fibrosis and cardiovascular disease

Award Number: R01HL185515
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 08/05/2026
PERIOD OF PERFORMANCE END DATE: 04/30/2031

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Multi-omic profiling of pulmonary fibrosis and cardiovascular disease - ABSTRACT Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease affecting 1 in 200 older adults, characterized by progressive lung scarring. Cardiovascular disease (CVD) is the second leading cause of death in IPF, and patients with IPF have a greater than threefold increased risk of acute coronary syndrome compared to the general population. This association is not fully explained by shared risk factors, and the mechanisms linking IPF and CVD remain poorly understood, representing a major barrier to the development of novel therapies for IPF. Our group has identified strong associations of vascular injury (ICAM1, VCAM1, P-selectin, D-dimer), dysregulated lipid handling (low HDL-C and apolipoprotein A1), and innate immune activation (monocytosis) with early pulmonary fibrosis and adverse outcomes. Our preliminary data show that individuals with co-existent subclinical pulmonary fibrosis and coronary artery calcium have significantly elevated levels of ICAM1 and monocytes, independent of age, sex, smoking, and adiposity. Our central hypothesis is that pulmonary fibrosis and CVD share molecular underpinnings characterized by vasculopathy, which drives accelerated disease progression and poor outcomes. The objective of this proposal is to identify the mechanisms underlying the relationship between CVD and IPF using multi-omic profiling of blood and tissue. We will leverage two NIH- funded programs, the Multi-Ethnic Study of Atherosclerosis (MESA) and PRECISIONS (large multi-site registry of patients with IPF and molecular characterization of blood samples using transcriptomics and proteomics) to perform the following aims: (1) define shared blood-based transcriptomic and proteomic signatures of comorbid IPF and CVD; (2): determine the association of a blood-based vasculo-fibrotic signature with IPF progression; and (3) identify shared cellular pathways in fibrotic lung and atherosclerotic plaque tissue using publicly available single-cell atlases. This study will uncover molecular mechanisms linking IPF and CVD, identify novel therapeutic targets, and enable potential repurposing of CVD-directed therapies to improve outcomes in IPF. By leveraging existing, rigorously phenotyped cohorts, the proposal is high-impact, feasible, and addresses a critical gap in the care of a high-risk population.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $768,414 )
2026	2026	WEILL MEDICAL COLLEGE OF CORNELL UNIVERSITY	575 LEXINGTON AVE FL 9	NEW YORK	NY	10022	NEW YORK	USA	Lung Diseases Research	000	1	8/12/2026	NEW	$768,414
														Subtotal = $768,414

Grand Total All Awards = $768,414

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Multi-omic profiling of pulmonary fibrosis and cardiovascular disease

Award Number: R01HL185515

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 08/05/2026

PERIOD OF PERFORMANCE END DATE: 04/30/2031

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