ArticleInternational journal of molecular sciences2024
GPR55 Antagonist CID16020046 Attenuates Obesity-Induced Airway Inflammation by Suppressing Chronic Low-Grade Inflammation in the Lungs.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Regulation of Cholesterol and Triglyceride Metabolism by Fatty acid Ethanolamides.Current atherosclerosis reports · 2026Review
- GPR55 Antagonist CID16020046 Suppresses Collagen-Induced Rheumatoid Arthritis by Suppressing Th1/Th17 Cells in Mice.International journal of molecular sciences · 2025Article
- Mechanistic insights into the PAI-1 inhibitor PAItrap3: enhancing lipid metabolism in adipose tissue of diabetic db/db mice.Frontiers in pharmacology · 2025Article
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Authors and funding
5 authors.
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Abstract
GPR55 is a receptor for lysophosphatidylinositols (LPIs) in digestive metabolites. Overnutrition leads to obesity, insulin resistance, and increased LPI levels in the plasma. The involvement of LPIs and GPR55 in adiposity, hepatic steatosis, and atherosclerosis has been previously elucidated. However, the therapeutic efficacy of GPR55 antagonists against obesity-induced airway inflammation has not been studied. The present study investigated whether CID16020046, a selective antagonist of GPR55, could modulate obesity-induced airway inflammation caused by a high-fat diet (HFD) in C57BL/6 mice. Administration of CID16020046 (1 mg/kg) inhibits HFD-induced adiposity and glucose intolerance. Analysis of immune cells in BALF showed that CID16020046 inhibited HFD-induced increase in immune cell infiltration. Histological analysis revealed the HFD induced hypersecretion of mucus and extensive fibrosis in the lungs. CID16020046 inhibited these HFD-induced pathological features. qRT-PCR revealed the HFD-induced increase in the expression of
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