# Distinct and Overlapping Pathways of Fibrosis and Emphysema in Cigarette Smokers

> **NIH NIH P01** · WEILL MEDICAL COLL OF CORNELL UNIV · 2021 · $2,658,770

## Abstract

PROJECT SUMMARY/ ABSTRACT
Cigarette smoking is the greatest known single risk factor for the development of lung disease, being a
dominant risk for the development of both emphysema and idiopathic pulmonary fibrosis. We have
assembled a team of investigators who have worked synergistically to better understand the mechanism(s)
by which cigarette smoke can induce either lung fibrosis or emphysema. Our team members are leaders in
the field of COPD and IPF who are most committed to better understand the mechanism(s) by which
cigarette smoke can induce either fibrotic or emphysematous phenotype in the lung. During the previous
years of funding support by P01 HL114501 grant entitled “Distinct and Overlapping Pathways of Fibrosis
and Emphysema in Cigarette Smokers”, we have integrated the expertise of investigators from the COPD
and IPF communities, spanning basic, translational and clinical researchers, to come together to tackle this
important challenge. This synergistic integration among the projects and cores have been impactful and will
continue to be greater than the sum of each of its component parts. We employ both Ureductionist and
mechanisticU approaches by utilizing cell culture and animal models (Project 1 and Project 2), and UdiscoveryU
approaches using high throughput profiling (genomics, epigenetics) methods in human lung tissues and
cells (Project 3) to discover new pathway(s) mediating the fibrotic and emphysema phenotypes in cigarette
smoker. Hence, a PPG mechanism has been not only critical but absolutely necessary to best address the
main objective of this fundamental question at hand: How can we better understand the mechanism(s) by
which cigarette smoke mediates fibrotic or emphysematous phenotype in the lung? We will attempt to reach
our goals by approaches described in the following Uprojects and cores:
Projects:
1) Mitochondrial and Metabolic Dysfunction in COPD and IPF
2) Differential roles of Chi3l1 and its Receptors in Pulmonary Fibrosis and COPD
3) Integrating Omics, Networks, and Functional Studies in COPD and IPF
Cores:
A) Administrative Core
B) Respiratory Computational Discovery Core
C) Clinical Biorepository Core
D) Molecular Characterization Core

## Key facts

- **NIH application ID:** 10172307
- **Project number:** 2P01HL114501-06A1
- **Recipient organization:** WEILL MEDICAL COLL OF CORNELL UNIV
- **Principal Investigator:** Augustine M Choi
- **Activity code:** P01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $2,658,770
- **Award type:** 2
- **Project period:** 2013-09-06 → 2026-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10172307

## Citation

> US National Institutes of Health, RePORTER application 10172307, Distinct and Overlapping Pathways of Fibrosis and Emphysema in Cigarette Smokers (2P01HL114501-06A1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10172307. Licensed CC0.

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