ArticleJCI insight2022
Chitinase 3 like 1 contributes to the development of pulmonary vascular remodeling in pulmonary hypertension.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Chitinase‑3 like‑protein‑1: A potential predictor of cardiovascular disease (Review).Molecular medicine reports · 2024Pooled it
- Astrocyte-oligodendrocyte crosstalk dependent myelination via secreted protein YKL40.bioRxiv : the preprint server for biology · 2026Article
- A Single-Cell Transcriptional Landscape of Emphysema: Heterogeneous Cellular Dynamics in Centrilobular, Panlobular, and Paraseptal Subtypes.International journal of molecular sciences · 2026Article
- CHI3L1: a novel regulator of vascular remodeling in pulmonary arterial hypertension.Molecular and cellular biochemistry · 2026Article
- The signature of pyroptosis-related gene diagnosis and immune microenvironment in preeclampsia.BMC pregnancy and childbirth · 2026Article
- [Silencing DDX17 inhibits proliferation and migration of pulmonary arterial smooth muscle cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Role of chitinase-3-like protein 1 in liver diseases: A comprehensive review.Genes & diseases · 2025Review
- Uncovering molecular markers of the microvascular endothelial response in sepsis-associated acute kidney injury: a translational study in mice and humans.Intensive care medicine experimental · 2025Article
- A new mechanism of arterial calcification in diabetes: interaction between H3K18 lactylation and CHI3L1.Clinical science (London, England : 1979) · 2025Article
- Mechanistic studies on the role of CHI3L1 in eosinophilic inflammation in chronic sinusitis.Frontiers in immunology · 2025Review
- Abnormally high expression of CHI3L1 in peripheral blood mononuclear cells and serum and their potential diagnosis and prediction from lymphoma patients.Frontiers in immunology · 2025Article
- Type 2 innate immunity promotes the development of pulmonary fibrosis in Hermansky-Pudlak syndrome.JCI insight · 2024Article
- Invasive growth of brain metastases is linked to CHI3L1 release from pSTAT3-positive astrocytes.Neuro-oncology · 2024Article
- Inhibition of Amyloid-β (Aβ)-Induced Cognitive Impairment and Neuroinflammation in CHI3L1 Knockout Mice through Downregulation of ERK-PTX3 Pathway.International journal of molecular sciences · 2024Article
- YKL-40 as a biomarker in various inflammatory diseases: A review.Biochemia medica · 2024Review
- Significance of chitinase-3-like protein 1 in the pathogenesis of inflammatory diseases and cancer.Experimental & molecular medicine · 2024Review
- Location-based prediction model for Crohn's disease regarding a novel serological marker, anti-chitinase 3-like 1 autoantibodies.World journal of gastroenterology · 2023Article
- Chitinase-3 like-protein-1, matrix metalloproteinase -9 and positive intracranial arterial remodelling.Frontiers in aging neuroscience · 2023Article
Corrections and comments
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Authors and funding
21 authors at 2 institutions in 1 country.
Funding
Abstract
Chitinase 3 like 1 (CHI3L1) is the prototypic chitinase-like protein mediating inflammation, cell proliferation, and tissue remodeling. Limited data suggest CHI3L1 is elevated in human pulmonary arterial hypertension (PAH) and is associated with disease severity. Despite its importance as a regulator of injury/repair responses, the relationship between CHI3L1 and pulmonary vascular remodeling is not well understood. We hypothesize that CHI3L1 and its signaling pathways contribute to the vascular remodeling responses that occur in pulmonary hypertension (PH). We examined the relationship of plasma CHI3L1 levels and severity of PH in patients with various forms of PH, including group 1 PAH and group 3 PH, and found that circulating levels of serum CHI3L1 were associated with worse hemodynamics and correlated directly with mean pulmonary artery pressure and pulmonary vascular resistance. We also used transgenic mice with constitutive knockout and inducible overexpression of CHI3L1 to examine its role in hypoxia-, monocrotaline-, and bleomycin-induced models of pulmonary vascular disease. In all 3 mouse models of pulmonary vascular disease, pulmonary hypertensive responses were mitigated in CHI3L1-null mice and accentuated in transgenic mice that overexpress CHI3L1. Finally, CHI3L1 alone was sufficient to induce pulmonary arterial smooth muscle cell proliferation, inhibit pulmonary vascular endothelial cell apoptosis, induce the loss of endothelial barrier function, and induce endothelial-mesenchymal transition. These findings demonstrate that CHI3L1 and its receptors play an integral role in pulmonary vascular disease pathobiology and may offer a target for the treatment of PAH and PH associated with fibrotic lung disease.
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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.