ArticleBiomolecules & therapeutics2020
Lodoxamide Attenuates Hepatic Fibrosis in Mice: Involvement of GPR35
Article in Biomolecules & therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Deciphering CD4+ Naive T cell-mediated divergent pathogenic links between type 2 diabetes and pathologic scarring via an integrated multi-omics approach.International journal of surgery (London, England) · 2026Article
- GPR35 prevents drug-induced liver injury via the Gαs-cAMP-PKA axis in macrophages.Cellular and molecular life sciences : CMLS · 2025Article
- GPR35-mediated metabolic reprogramming promotes tumorigenesis in digestive cancers.Frontiers in immunology · 2025Review
- GPR35 acts a dual role and therapeutic target in inflammation.Frontiers in immunology · 2023Review
- Exercised accelerated the production of muscle-derived kynurenic acid in skeletal muscle and alleviated the postmenopausal osteoporosis through the Gpr35/NFκB p65 pathway.Journal of orthopaedic translation · 2022Article
- G Protein-Coupled Receptor GPR35 Suppresses Lipid Accumulation in Hepatocytes.ACS pharmacology & translational science · 2021Article
- GPR35 in Intestinal Diseases: From Risk Gene to Function.Frontiers in immunology · 2021Review
- Therapeutic Opportunities and Challenges in Targeting the Orphan G Protein-Coupled Receptor GPR35.ACS pharmacology & translational science · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A previous pharmacogenomic analysis identified cromolyn, an anti-allergic drug, as an effective anti-fibrotic agent that acts on hepatocytes and stellate cells. Furthermore, cromolyn was shown to be a G protein-coupled receptor 35 (GPR35) agonist. However, it has not been studied whether anti-fibrotic effects are mediated by GPR35. Therefore, in this study, the role of GPR35 in hepatic fibrosis was investigated through the use of lodoxamide, another anti-allergic drug and a potent GPR35 agonist. Longterm treatment with carbon tetrachloride induced hepatic fibrosis, which was inhibited by treatment with lodoxamide. Furthermore, CID2745687, a specific GPR35 antagonist, reversed lodoxamide-mediated anti-fibrotic effects. In addition, lodoxamide treatment showed significant effects on the mRNA expression of collagen Iα1, collagen Iα2, and TGF-β1 in the extracellular matrix. However, a transforming growth factor α (TGF-α) shedding assay revealed lodoxamide not to be a potent agonist of mouse GPR35
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