ArticleFrontiers in medicine2022
Targeting acid ceramidase ameliorates fibrosis in mouse models of non-alcoholic steatohepatitis.
Article in Frontiers in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Deep behavioral phenotyping reveals novel features in a mouse model of metabolic dysfunction-associated steatohepatitis.Scientific reports · 2026Article
- Resolving fibrosis by stimulating HSC-dependent extracellular matrix degradation.Science translational medicine · 2025Article
- Noncanonical role of Golgi-associated macrophage TAZ in chronic inflammation and tumorigenesis.Science advances · 2025Article
- Correlation between liver fibrosis in non-alcoholic fatty liver disease and insulin resistance indicators: a cross-sectional study from NHANES 2017-2020.Frontiers in endocrinology · 2025Article
- Cardiac dysfunction and altered gene expression in acid ceramidase-deficient mice.American journal of physiology. Heart and circulatory physiology · 2025Article
- Acid Ceramidase Deficiency: Bridging Gaps between Clinical Presentation, Mouse Models, and Future Therapeutic Interventions.Biomolecules · 2023Review
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
Non-alcoholic fatty liver disease (NAFLD) is a common cause of liver disease worldwide, and is characterized by the accumulation of fat in the liver. Non-alcoholic steatohepatitis (NASH), an advanced form of NAFLD, is a leading cause of liver transplantation. Fibrosis is the histologic feature most associated with liver-related morbidity and mortality in patients with NASH, and treatment options remain limited. In previous studies, we discovered that acid ceramidase (aCDase) is a potent antifibrotic target using human hepatic stellate cells (HSCs) and models of hepatic fibrogenesis. Using two dietary mouse models, we demonstrate that depletion of aCDase in HSC reduces fibrosis without worsening metabolic features of NASH, including steatosis, inflammation, and insulin resistance. Consistently, pharmacologic inhibition of aCDase ameliorates fibrosis but does not alter metabolic parameters. The findings suggest that targeting aCDase is a viable therapeutic option to reduce fibrosis in patients with NASH.
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