ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
β-sitosterol attenuates hepatic lipid accumulation and fibrosis via NLRP3 signaling in MASH mice.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
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
3 citing papers in PubMed.
- Ginseng nonsaponins: New insights into their pharmacological potentials in inflammasome-driven inflammation and immunopathology.Journal of ginseng research · 2026Review
- Molecular genetic basis and clinical heterogeneity of sitosterolemia: focusing on the mutation spectrum and pathogenic mechanisms of ABCG5/ABCG8 genes.Frontiers in nutrition · 2026Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Β-sitosterol (SIT), a natural phytosterol, has not been fully explored for its therapeutic potential in metabolic dysfunction-associated steatohepatitis (MASH). In this study, MASH was induced in mice via a high-fat, high-cholesterol (HFHC) diet, and lipid accumulation in HepG2 cells was triggered with oleic acid (OA), while the role of the NLRP3 inflammasome was explored in NLRP3-knockout (NLRP3
Indexed as
Identifiers
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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.