ArticleJournal of inflammation research2022
Pharmacological Inhibition of Chitotriosidase (CHIT1) as a Novel Therapeutic Approach for Sarcoidosis.
Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- New Therapies for Sarcoidosis: Molecular and Pathophysiological Basis.International journal of molecular sciences · 2026Review
- Identification of a distinctive gene signature associated with disease activity in granulomatous myositis.Rheumatology (Oxford, England) · 2026Article
- Elevated levels of cerebrospinal fluid CHIT1 correlate with disease activity in neuromyelitis optica spectrum disorder.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Elucidation of the Catalytic Apparatus and Mechanism of Human Chitotriosidase‑1.ACS catalysis · 2025Article
- Myopathology and Immune Profile of Granulomatous Myositis in Sarcoid Myopathy.Neuropathology and applied neurobiology · 2025Article
- Human chitinases and chitinase-like proteins as emerging drug targets - a medicinal chemistry perspective.RSC medicinal chemistry · 2025Review
- Chitinase-1 inhibition attenuates metabolic dysregulation and restores homeostasis in MASH animal models.Frontiers in immunology · 2025Article
- Genomic Insights into Idiopathic Granulomatous Mastitis through Whole-Exome Sequencing: A Case Report of Eight Patients.International journal of molecular sciences · 2024Article
- Multiomic analysis of monocyte-derived alveolar macrophages in idiopathic pulmonary fibrosis.Journal of translational medicine · 2024Article
- Serum chitotriosidase activity in South African patients with sarcoidosis and tuberculosis.African journal of thoracic and critical care medicine · 2024Article
- Metabolism-driven glycosylation represents therapeutic opportunities in interstitial lung diseases.Frontiers in immunology · 2024Review
- Inhibition of Macrophage-Specific CHIT1 as an Approach to Treat Airway Remodeling in Severe Asthma.International journal of molecular sciences · 2023Article
- Macrophage Biology in Human Granulomatous Skin Inflammation.International journal of molecular sciences · 2023Review
- The Role of Chitinases in Chronic Airway Inflammation Associated with Tobacco Smoke Exposure.Cells · 2022Article
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Sarcoidosis is a systemic disease of unknown etiology characterized by granuloma formation in the affected tissues. The pathologically activated macrophages are causatively implicated in disease pathogenesis and play important role in granuloma formation. Chitotriosidase (CHIT1), macrophage-derived protein, is upregulated in sarcoidosis and its levels correlate with disease severity implicating CHIT1 in pathology. Methods: CHIT1 was evaluated in serum and bronchial mucosa and mediastinal lymph nodes specimens from sarcoidosis patients. The therapeutic efficacy of OATD-01 was assessed ex vivo on human bronchoalveolar lavage fluid (BALF) macrophages and in vivo in the murine models of granulomatous inflammation. Results: CHIT1 activity was significantly upregulated in serum from sarcoidosis patients. CHIT1 expression was restricted to granulomas and localized in macrophages. Ex vivo OATD-01 inhibited pro-inflammatory mediators' production (CCL4, IL-15) by lung macrophages. In the acute model of granulomatous inflammation in mice, OATD-01 showed anti-inflammatory effects reducing the percentage of neutrophils and CCL4 concentration in BALF. In the chronic model, inhibition of CHIT1 led to a decrease in the number of organized lung granulomas and the expression of sarcoidosis-associated genes. Conclusion: In summary, CHIT1 activity was increased in sarcoidosis patients and OATD-01, a first-in-class CHIT1 inhibitor, demonstrated efficacy in murine models of granulomatous inflammation providing a proof-of-concept for its clinical evaluation in sarcoidosis.
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