ArticleACS pharmacology & translational science2021
G Protein-Coupled Receptor GPR35 Suppresses Lipid Accumulation in Hepatocytes.
Article in ACS pharmacology & translational science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Receptor-Mitochondria Crosstalk in the Kynurenine Metabolic Pathway: Integrating Metabolomics and Clinical Mass Spectrometry.Antioxidants (Basel, Switzerland) · 2026Review
- G protein-coupled receptor 35 stimulation reduces osteoclast activity in primary human bone cells.JBMR plus · 2025Article
- Processed silkworm powder (Hongjam) ameliorates metabolic dysfunction-associated steatotic liver disease via GPR35/PKA and SIRT1/AMPK pathways.Frontiers in nutrition · 2025Article
- GPR35-mediated metabolic reprogramming promotes tumorigenesis in digestive cancers.Frontiers in immunology · 2025Review
- Spatial multi-omics characterizes GPR35-relevant lipid metabolism signatures across liver zonation in MASLD.Life metabolism · 2024Article
- From orphan to oncogene: The role of GPR35 in cancer and immune modulation.Cytokine & growth factor reviews · 2024Review
- Article
- Recent advances in GPR35 pharmacology; 5-HIAA serotonin metabolite becomes a ligand.Archives of pharmacal research · 2023Review
- Effect ofAnimals : an open access journal from MDPI · 2023Article
- G protein-coupled receptor 35 attenuates nonalcoholic steatohepatitis by reprogramming cholesterol homeostasis in hepatocytes.Acta pharmaceutica Sinica. B · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although prevalent, nonalcoholic fatty liver disease is not currently treated effectively with medicines. Initially, using wild-type and genome-edited clones of the human hepatocyte cell line HepG2, we show that activation of the orphan G protein-coupled receptor GPR35 is both able and sufficient to block liver X-receptor-mediated lipid accumulation. Studies on hepatocytes isolated from both wild-type and GPR35 knock-out mice were consistent with a similar effect of GPR35 agonists in these cells, but because of marked differences in the pharmacology of GPR35 agonists and antagonists at the mouse and human orthologues, as well as elevated basal lipid levels in hepatocytes from the GPR35 knock-out mice, no definitive conclusion could be reached. To overcome this, we generated and characterized a transgenic knock-in mouse line in which the corresponding human GPR35 splice variant replaced the mouse orthologue. In hepatocytes from these humanized GPR35 mice, activation of this receptor was shown conclusively to prevent, and also reverse, lipid accumulation induced by liver X-receptor stimulation. These studies highlight the potential to target GPR35 in the context of fatty liver diseases.
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Registered trials
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