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Chitinase 3-like 1 suppresses injury and promotes fibroproliferative responses in Mammalian lung fibrosis
Open accessAbstract
Chitinase 3–like 1 protects against lung injury but has a profibrotic role during the repair phase.
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“a relative excess of M1 macrophages leads to epithelial cell death and failure of repair such as that seen in acute exacerbation of IPF (AE-IPF)”
From The Role of Immune and Inflammatory Cells in Idiopathic Pulmonary Fibrosis (2018) · cites this paper as [21]
In the citing paper
“an excess of M2 macrophages leads to the aberrant and dysregulated repair responses that characterize progressive fibrosis (21)”
From The Role of Immune and Inflammatory Cells in Idiopathic Pulmonary Fibrosis (2018) · cites this paper as [21]
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Metadata
- Authors
- Zhou, Y., Peng, H., Sun, H., Peng, X., Tang, C., Gan, Y., Chen, X., Mathur, A., Hu, B., Slade, M. D., Montgomery, R. R., Shaw, A. C., Homer, R. J., White, E. S., Lee, C.-M., Moore, M. W., Gulati, M., Geun Lee, C., Elias, J. A., & Herzog, E. L.
- Affiliations
- Yale University (US)
- Second Xiangya Hospital of Central South University (CN)
- University of Michigan (US)
- Section of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
- Brown University (US)
- Corresponding author
- Zhou, Yang
- Peng, Hong
- Sun, Huanxing
- Elias, Jack A.
- Herzog, Erica L.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2014-06-11
- Volume
- 6
- Issue
- 240
- Pages
- 240ra76-240ra76
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC4340473
- OpenAlex
- W2159203930
- Cited by
- 215
- References
- 64
- Citations by year
- 2026: 12 · 2025: 21 · 2024: 21 · 2023: 17 · 2022: 23 · 2021: 34 · 2020: 14 · 2019: 13 · 2018: 17 · 2017: 16 · 2016: 8 · 2015: 14 · 2014: 4
- FWCI
- 11.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR000142)
- U.S. Public Health Service (N01-HHS N272201100019C)
- National Institute on Aging (K24AG042489)
- National Heart, Lung, and Blood Institute (R01HL093017, U01HL108638, U01HL111016, U01HL112702, R01HL109233, HL-109033, R01HL109118, HL093017, U01HL109118, R01HL085083, P01HL114501, T32HL007749)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Studies on Chitinases and Chitosanases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
- Keywords
- YKL-40, idiopathic pulmonary fibrosis, pulmonary fibrosis, epithelial damage, fibroproliferation, alternative macrophage activation, myofibroblast transformation, fibroblast proliferation, apoptosis, disease progression, acute exacerbation, bleomycin-induced lung injury, circulating monocytes, extracellular matrix deposition, inflammation
- MeSH terms
- Chitinase-3-Like Protein 1, Animals, Enzyme-Linked Immunosorbent Assay, Female, Fibroblasts, Flow Cytometry, Humans, Lung, Pulmonary Fibrosis, Bone Marrow Transplantation, Apoptosis, Mice, Knockout, In Situ Nick-End Labeling, Lectins, Cell Proliferation, Mice, Adipokines
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