ArticleClinical and molecular hepatology2023
Taurocholic acid promotes hepatic stellate cell activation via S1PR2/p38 MAPK/YAP signaling under cholestatic conditions.
Article in Clinical and molecular hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 50 citations in OpenAlex.
- Contribution of p38 MAPK in liver fibrosis: An overview of mechanisms, signaling pathways, and therapeutic targets (Review).International journal of molecular medicine · 2026Review
- From network prediction to in vivo validation: luteolin attenuates cholestatic liver injury in association with PI3K/Akt/GSK-3β signalling modulation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Alcohol-related liver disease disrupts bile acid homeostasis and gut microbial bile acid metabolism.JHEP reports : innovation in hepatology · 2026Article
- NUP85 Mediates Endoplasmic Reticulum Stress through the USP47/ASK1 Signaling Pathway to Regulate the Progression of Liver Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A metabolite-augmented FIB-4 machine learning panel achieves superior liver fibrosis staging in chronic liver disease.Cell reports. Medicine · 2026Article
- Liver Stiffness Rises Early in MASLD and Drives Inflammation, Lipid Dysmetabolism, and Fibrosis via Piezo1-YAP Mechanotransduction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Underestimated and Overlooked Factors in PBC Progression: Bacterial and Fungal Infections.International journal of molecular sciences · 2026Review
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Gut microbiome and bile acid metabolism in liver disease: Mechanisms, clinical implications, and therapeutic opportunities.Pharmacological reviews · 2026Review
- Taurocholic Acid Is Associated With Disturbed Functional Connectivity in the Hippocampus of Patients With Depression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Observational
- Metamorphosing macrophages promote placental fibrosis by upregulating the transcription factor STAT5A.Journal of translational medicine · 2026Article
- Sleep Deprivation Promotes Colorectal Cancer in ApcInternational journal of biological sciences · 2026Article
- Regulation of bile acids homeostasis: a feasible and versatile way to treat or diagnose liver disorders.Frontiers in nutrition · 2026Review
- Bile acid signaling: from dynamic pool composition to inter-organ communication.Frontiers in endocrinology · 2026Review
- GCDCA promotes hepatocellular carcinoma progression through S1PR2/PI3K/AKT-mediated polarization of M2-type macrophages.Frontiers in immunology · 2026Article
- Natural drugs modulate MAPK: targets and strategies for liver fibrosis treatment.Frontiers in pharmacology · 2026Review
- Therapeutic modulation of the gut microbiota by traditional Chinese medicine in the management of cholestatic liver injury.Frontiers in cellular and infection microbiology · 2026Review
- From chemical composition to clinical application: the value of bile-based traditional Chinese medicines in the treatment of liver diseases.Frontiers in pharmacology · 2026Review
- Regulatory effects of Sini-San on bile acid homeostasis in the enterohepatic circulation of mice with liver fibrosis.Chinese medicine · 2025Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimsDisrupted bile acid regulation and accumulation in the liver can contribute to progressive liver damage and fibrosis. However, the effects of bile acids on the activation of hepatic stellate cells (HSCs) remain unclear. This study investigated the effects of bile acids on HSC activation during liver fibrosis, and examined the underlying mechanisms.
methodsThe immortalized HSCs, LX-2 and JS-1cells were used for the in vitro study. in vitro, the adeno-associated viruses adeno-associated virus-sh-S1PR2 and JTE-013 were used to pharmacologically inhibit the activity of S1PR2 in a murine model of fibrosis induced by a 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet. Histological and biochemical analyses were performed to study the involvement of S1PR2 in the regulation of fibrogenic factors as well as the activation properties of HSCs.
resultsS1PR2 was the predominant S1PR expressed in HSCs and was upregulated during taurocholic acid (TCA) stimulation and in cholestatic liver fibrosis mice. TCA-induced HSC proliferation, migration and contraction and extracellular matrix protein secretion were inhibited by JTE-013 and a specific shRNA targeting S1PR2 in LX-2 and JS-1 cells. Meanwhile, treatment with JTE-013 or S1PR2 deficiency significantly attenuated liver histopathological injury, collagen accumulation, and the expression of fibrogenesis-associated genes in mice fed a DDC diet. Furthermore, TCAmediated activation of HSCs through S1PR2 was closely related to the yes-associated protein (YAP) signaling pathway via p38 mitogen-activated protein kinase (p38 MAPK).
conclusionTCA-induced activation of the S1PR2/p38 MAPK/YAP signaling pathways plays a vital role in regulating HSC activation, which might be therapeutically relevant for targeting cholestatic liver fibrosis.
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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.