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Chitinase 3-like 1 suppresses injury and promotes fibroproliferative responses in Mammalian lung fibrosis
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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]
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“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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