ArticlePloS one2024
Sphingosine-1-phosphate promotes liver fibrosis in metabolic dysfunction-associated steatohepatitis.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Metabolic dysfunction-associated steatohepatitis (MASH): intersections with type 2 diabetes and insulin resistance.Frontiers in endocrinology · 2026Pooled it
- Sphingolipid homeostasis and dysregulation in liver function and disease.Life metabolism · 2026Review
- Integrative multi-omics analyses reveal the molecular mechanisms of lysozyme in alleviating hepatic lipid accumulation in post-peak laying quail.Poultry science · 2026Article
- F13A1-Mediated Macrophage Activation Promotes MASH Progression via the PKM2/HIF1A Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting SPHK1 by 8-HETrE attenuates MASH-Driven fibrosis via restoration of hepatic stellate cell mitochondrial dynamics.Cell biology and toxicology · 2026Article
- Ceramidase is involved in metabolic reprogramming of fibroblasts under hypoxia conditions.Frontiers in physiology · 2026Article
- Autoimmunity in MASLD: Focus on autoantibodies, anti-apolipoprotein A1 IgG and G protein-coupled receptors.European journal of clinical investigation · 2025Review
- Extracellular Vesicles as Biomarkers in Chronic Hepatobiliary Diseases: An Overview of Their Interplay.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimMetabolic dysfunction-associated steatohepatitis (MASH) is one of the most prevalent liver diseases and is characterized by steatosis and the accumulation of bioactive lipids. This study aims to understand the specific lipid species responsible for the progression of liver fibrosis in MASH.
methodsChanges in bioactive lipid levels were examined in the livers of MASH mice fed a choline-deficient diet (CDD). Additionally, sphingosine kinase (SphK)1 mRNA, which generates sphingosine 1 phosphate (S1P), was examined in the livers of patients with MASH.
resultsCDD induced MASH and liver fibrosis were accompanied by elevated levels of S1P and increased expression of SphK1 in capillarized liver sinusoidal endothelial cells (LSECs) in mice. SphK1 mRNA also increased in the livers of patients with MASH. Treatment of primary cultured mouse hepatic stellate cells (HSCs) with S1P stimulated their activation, which was mitigated by the S1P receptor (S1PR)2 inhibitor, JTE013. The inhibition of S1PR2 or its knockout in mice suppressed liver fibrosis without reducing steatosis or hepatocellular damage.
conclusionS1P level is increased in MASH livers and contributes to liver fibrosis via S1PR2.
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