ArticleJCI insight2023
Medium-chain fatty acids suppress lipotoxicity-induced hepatic fibrosis via the immunomodulating receptor GPR84.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Pharmacological modulation of GPR84 revealed by dual states structures and immune functional assays.Experimental & molecular medicine · 2026Article
- Mechanistic insight into signal bias by the agonist-dependent conformational dynamics of GPR84.Nature communications · 2026Article
- Review
- GPR84 aggravates lung inflammation through activating ZBP1-PANoptosome mediated PANoptosis following IAV infection.Cell death discovery · 2026Article
- Article
- A Lipid Road to Neuroimmunology: Fatty Acids Linking Immune and Nervous Systems.Neuroimmunomodulation · 2026Review
- Orphan GPCRs in diabetes mellitus: metabolic control, inflammation, and drug development.Frontiers in endocrinology · 2026Review
- The free fatty acid receptor GPR164 maintains intestinal homeostasis and barrier function.EMBO reports · 2025Article
- Article
- Targeting GPR84 to alleviate acute immune-mediated liver injury.Molecular medicine (Cambridge, Mass.) · 2025Article
- A medium-chain fatty acid analogue prevents endotoxin liver injury in a murine model.Scientific reports · 2025Article
- Machine learning-based models for advanced fibrosis in non-alcoholic steatohepatitis patients: A cohort study.World journal of gastroenterology · 2025Article
- Mycobacteria Exploit Host GPR84 to Dampen Pro-Inflammatory Responses and Promote Infection in Macrophages.Microorganisms · 2025Article
- Distinct changes in serum metabolites and lipid species in the onset and progression of NAFLD in Obese Chinese.Computational and structural biotechnology journal · 2024Article
- Article
- Medium-chain fatty acid receptor GPR84 deficiency leads to metabolic homeostasis dysfunction in mice fed high-fat diet.FASEB bioAdvances · 2024Article
- Non-invasive SARS-CoV-2 RNA detection and human transcriptome analysis using skin surface lipids.Scientific reports · 2024Article
- A high-fat diet supplemented with medium-chain triglycerides ameliorates hepatic steatosis by reducing ceramide and diacylglycerol accumulation in mice.Experimental physiology · 2024Article
- Development of Highly Potent, G-Protein Pathway Biased, Selective, and Orally Bioavailable GPR84 Agonists.Journal of medicinal chemistry · 2024Article
- Insulin Resistance, Obesity, and Lipotoxicity.Advances in experimental medicine and biology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Medium-chain triglycerides (MCTs), which consist of medium-chain fatty acids (MCFAs), are unique forms of dietary fat with various health benefits. G protein-coupled 84 (GPR84) acts as a receptor for MCFAs (especially C10:0 and C12:0); however, GPR84 is still considered an orphan receptor, and the nutritional signaling of endogenous and dietary MCFAs via GPR84 remains unclear. Here, we showed that endogenous MCFA-mediated GPR84 signaling protected hepatic functions from diet-induced lipotoxicity. Under high-fat diet (HFD) conditions, GPR84-deficient mice exhibited nonalcoholic steatohepatitis (NASH) and the progression of hepatic fibrosis but not steatosis. With markedly increased hepatic MCFA levels under HFD, GPR84 suppressed lipotoxicity-induced macrophage overactivation. Thus, GPR84 is an immunomodulating receptor that suppresses excessive dietary fat intake-induced toxicity by sensing increases in MCFAs. Additionally, administering MCTs, MCFAs (C10:0 or C12:0, but not C8:0), or GPR84 agonists effectively improved NASH in mouse models. Therefore, exogenous GPR84 stimulation is a potential strategy for treating NASH.
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Registered trials
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 Socratic graph.