Inhibition of Glutaminase 1 Attenuates Experimental Pulmonary Fibrosis
Open accessAbstract
It has been increasingly recognized lately that aberrant cellular metabolism plays an important role in the pathogenesis of pulmonary fibrosis. In our previous systemic studies, we found that human lung myofibroblasts undergo glutaminolytic reprogramming, which is mediated by an increased expression of glutaminase (Gls) 1. We showed that augmented glutaminolysis critically regulates collagen production by promoting its stabilization in human lung myofibroblasts. Our study indicates that lung fibroblast Gls1 is a promising therapeutic target for this disease. In this investigation, we primarily focused on delineating the in vivo role of fibroblast Gls1 in mouse models of pulmonary fibrosis and determining the efficacy of Gls1 inhibition in treating this pathology. We now show that fibroblast Gls1 is upregulated in fibrotic mouse lungs. We present evidence that mice with ablation of fibroblast Gls1 are protected from bleomycin-induced lung fibrosis. We show that the Gls1 inhibitor, CB-839, is therapeutically efficacious in treating both bleomycin- and transforming growth factor-β1–induced pulmonary fibrosis. Our study has thus established a solid rationale for advancing Gls1 inhibitors, particularly CB-839, to the next stage of testing in the treatment of this disease.
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Gata6+ macrophages are present in human pericardial fluid, suggesting that this immune cardioprotective role for the pericardial tissue compartment may be relevant in human disease.
“Gata6+ macrophages were also present in human pericardial fluid, suggesting that this immune cardioprotective role for the pericardial tissue compartment may be relevant in human disease73.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [73]
Following myocardial infarction in mice, Gata6+ macrophages in mouse pericardial fluid invade the epicardium and lose Gata6 expression but maintain anti-fibrotic properties, and loss of this macrophage population enhances interstitial fibrosis after ischemic injury.
“Following myocardial infarction in mice, Gata6+ macrophages in mouse pericardial fluid invaded the epicardium and lost Gata6 expression but maintained anti-fibrotic properties, and loss of this macrophage population enhanced interstitial fibrosis post-ischemic injury.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [73]
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Research works printed but not linked: 5
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- Authors
- Cui, H., Xie, N., Jiang, D., Banerjee, S., Ge, J., Sanders, Y. Y., & Liu, G.
- Affiliations
- University of Alabama at Birmingham (US)
- China-Japan Friendship Hospital (CN)
- Corresponding author
- Liu, Gang
- Venue
- American Journal of Respiratory Cell and Molecular Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-10-01
- Volume
- 61
- Issue
- 4
- Pages
- 492-500
- ISSN
- 1044-1549 (ISSN-L)
- 1535-4989
- PMC
- PMC6775943
- OpenAlex
- W2928749667
- Cited by
- 76
- References
- 34
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 9 · 2023: 9 · 2022: 12 · 2021: 11 · 2020: 8 · 2019: 3
- FWCI
- 6.25
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Respiratory Cell and Molecular Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R01AG050567)
- National Heart, Lung, and Blood Institute (R01HL126737, R35HL135830)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
- Health Sciences › Medicine › Surgery › Transplantation: Methods and Outcomes
- Keywords
- pulmonary fibrosis, GLS1, glutaminolysis, lung fibroblasts, myofibroblasts, CB-839, bleomycin-induced lung fibrosis, TGF-β1, collagen synthesis, cellular metabolism, therapeutic target
- MeSH terms
- Animals, Bleomycin, Cell Line, Collagen, Enzyme Induction, Fibroblasts, Glutaminase, Lung, Male, Mice, Inbred C57BL, Pulmonary Fibrosis, RNA, Messenger, Thiadiazoles, RNA Interference, RNA, Small Interfering, Benzeneacetamides, Mice, Transforming Growth Factor beta1, Molecular Targeted Therapy
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