ArticleAmerican journal of respiratory cell and molecular biology2022
CRTH2 Mediates Profibrotic Macrophage Differentiation and Promotes Lung Fibrosis.
Article in American journal of respiratory cell and molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Neuropsychiatric disorders in pulmonary fibrosis: from brain network alterations to inflammatory mechanisms and therapeutic implications.Journal of neuroinflammation · 2026Review
- Monocyte LOXHD1 and RHOB Expression Predictive of Progressive Systemic Sclerosis-Associated Interstitial Lung Disease.Arthritis care & research · 2026Article
- [Research progress on serum chitinase-3-like protein 1 for diagnosing early-stage liver fibrosis non-invasively].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025Review
- Role of chitinase-3-like protein 1 in liver diseases: A comprehensive review.Genes & diseases · 2025Review
- RTN3 regulates collagen biosynthesis and profibrotic macrophage differentiation to promote pulmonary fibrosis via interacting with CRTH2.Molecular medicine (Cambridge, Mass.) · 2025Article
- Molecular basis of lipid and ligand regulation of prostaglandin receptor DP2.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Inflammatory Effects and Regulatory Mechanisms of Chitinase-3-like-1 in Multiple Human Body Systems: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Endogenous PGD2 acting on DP2 receptor counter regulates Schistosoma mansoni infection-driven hepatic granulomatous fibrosis.PLoS pathogens · 2024Article
- Uncovering novel mechanisms of chitinase-3-like protein 1 in driving inflammation-associated cancers.Cancer cell international · 2024Review
- Review
- Osteopontin: an essential regulatory protein in idiopathic pulmonary fibrosis.Journal of molecular histology · 2024Review
- Progress and Gaps in Respiratory Disease Research and Treatment: Highlights of the IRM 2024 in Shanghai.Journal of respiratory biology and translational medicine · 2024Article
- Review
- Chitinase 3 like 1 contributes to the development of pulmonary vascular remodeling in pulmonary hypertension.JCI insight · 2022Article
- Biology of lung macrophages in health and disease.Immunity · 2022Review
- CRTH2 in Pulmonary Fibrosis: Friend or Foe?American journal of respiratory cell and molecular biology · 2022Article
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a particularly deadly form of pulmonary fibrosis of unknown cause. In patients with IPF, high serum and lung concentrations of CHI3L1 (chitinase 3 like 1) can be detected and are associated with poor survival. However, the roles of CHI3L1 in these diseases have not been fully elucidated. We hypothesize that CHI3L1 interacts with CRTH2 (chemoattractant receptor-homologous molecule expressed on T-helper type 2 cells) to stimulate profibrotic macrophage differentiation and the development of pulmonary fibrosis and that circulating blood monocytes from patients with IPF are hyperresponsive to CHI3L1-CRTH2 signaling. We used murine pulmonary fibrosis models to investigate the role of CRTH2 in profibrotic macrophage differentiation and fibrosis development and primary human peripheral blood mononuclear cell culture to detect the difference of monocytes in the responses to CHI3L1 stimulation and CRTH2 inhibition between patients with IPF and normal control subjects. Our results showed that null mutation or small-molecule inhibition of CRTH2 prevents the development of pulmonary fibrosis in murine models. Furthermore, CHI3L1 stimulation induces a greater increase in CD206 expression in IPF monocytes than control monocytes. These results demonstrated that monocytes from patients with IPF appear to be hyperresponsive to CHI3L1 stimulation. These studies support targeting the CHI3L1-CRTH2 pathway as a promising therapeutic approach for IPF and that the sensitivity of blood monocytes to CHI3L1-induced profibrotic differentiation may serve as a biomarker that predicts responsiveness to CHI3L1- or CRTH2-based interventions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.