ArticleJournal of immunology research2018
Deoxycholic Acid-Mediated Sphingosine-1-Phosphate Receptor 2 Signaling Exacerbates DSS-Induced Colitis through Promoting Cathepsin B Release.
Article in Journal of immunology research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
- Bile salt hydrolase activity as a rational target for MASLD therapy.Gut microbes · 2026Article
- Glycodeoxycholic acid inhibits hepatocellular carcinoma by driving M1 polarization of macrophages via the S1PR2-NF-κB-NLRP3 pathway.JHEP reports : innovation in hepatology · 2026Article
- Decoding the gut microbiota-mitochondrial-inflammasome axis in cardiovascular disease.Molecular and cellular biochemistry · 2026Review
- Hyodeoxycholic Acid Suppresses High-Fat-Diet-Promoted MC38-Syngeneic Colorectal Tumor Growth via Bile Acid Remodeling and Microbiota Modulation.Nutrients · 2025Article
- 7-Ketodeoxycholic Acid Promotes Colonic Mucosal Healing by Inducing Calcium Release from Endoplasmic Reticulum via the TGR5-IP3R Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Bile acid-microbiota interactions in cardiometabolic diseases: mechanisms and emerging therapeutic approaches.Frontiers in microbiology · 2025Review
- Review
- Bile Acid Signaling in Metabolic and Inflammatory Diseases and Drug Development.Pharmacological reviews · 2024Review
- Bile acid-sensitive human norovirus strains are susceptible to sphingosine-1-phosphate receptor 2 inhibition.Journal of virology · 2024Article
- Bidirectional two-sample Mendelian randomization analysis investigates causal associations between cathepsins and inflammatory bowel disease.Frontiers in genetics · 2024Article
- Bile acids and their receptors: Potential therapeutic targets in inflammatory bowel disease.World journal of gastroenterology · 2023Review
- Emerging Roles of Gut Microbial Modulation of Bile Acid Composition in the Etiology of Cardiovascular Diseases.Nutrients · 2023Review
- Inhibition of Sphingosine-1-Phosphate Receptor 2 by JTE013 Enhanced Alveolar Bone Regeneration by Promoting Angiogenesis.International journal of molecular sciences · 2023Article
- Unveiling the biological role of sphingosine-1-phosphate receptor modulators in inflammatory bowel diseases.World journal of gastroenterology · 2023Review
- Farnesoid X receptor antagonizes macrophage-dependent licensing of effector T lymphocytes and progression of sclerosing cholangitis.Science translational medicine · 2022Article
- Bile Acids: Physiological Activity and Perspectives of Using in Clinical and Laboratory Diagnostics.Molecules (Basel, Switzerland) · 2022Review
- New Insights into Bile Acids Related Signaling Pathways in the Onset of Colorectal Cancer.Nutrients · 2022Review
- Bile acid coordinates microbiota homeostasis and systemic immunometabolism in cardiometabolic diseases.Acta pharmaceutica Sinica. B · 2022Review
- Genetic manipulation of gut microbes enables single-gene interrogation in a complex microbiome.Cell · 2022Article
- Inflammatory-Dependent Bidirectional Effect of Bile Acids on NLRP3 Inflammasome and Its Role in Ameliorating CPT-11-Induced Colitis.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently have proved that excessive fecal DCA caused by high-fat diet may serve as an endogenous danger-associated molecular pattern to activate NLRP3 inflammasome and thus contributes to the development of inflammatory bowel disease (IBD). Moreover, the effect of DCA on inflammasome activation is mainly mediated through bile acid receptor sphingosine-1-phosphate receptor 2 (S1PR2); however, the intermediate process remains unclear. Here, we sought to explore the detailed molecular mechanism involved and examine the effect of S1PR2 blockage in a colitis mouse model. In this study, we found that DCA could dose dependently upregulate S1PR2 expression. Meanwhile, DCA-induced NLRP3 inflammasome activation is at least partially achieved through stimulating extracellular regulated protein kinases (ERK) signaling pathway downstream of S1PR2 followed by promoting of lysosomal cathepsin B release. DCA enema significantly aggravated DSS-induced colitis in mice and S1PR2 inhibitor as well as inflammasome inhibition by cathepsin B antagonist substantially reducing the mature IL-1
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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 OpenQuestion graph.