ArticleJournal of food and drug analysis2019
CCM111 prevents hepatic fibrosis via cooperative inhibition of TGF-β, Wnt and STAT3 signaling pathways.
Article in Journal of food and drug analysis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Analysis of risk factors and correlation between the degree of hepatic steatosis and fibrosis in patients with metabolic dysfunction-associated steatohepatitis.BMC gastroenterology · 2025Article
- Antioxidant therapy against TGF-β/SMAD pathway involved in organ fibrosis.Journal of cellular and molecular medicine · 2024Review
- Signaling pathways that activate hepatic stellate cells during liver fibrosis.Frontiers in medicine · 2024Review
- Daucosterol Alleviates Alcohol-Induced Hepatic Injury and Inflammation through P38/NF-κB/NLRP3 Inflammasome Pathway.Nutrients · 2023Article
- Lycorine Ameliorates Thioacetamide-Induced Hepatic Fibrosis in Rats: Emphasis on Antioxidant, Anti-Inflammatory, and STAT3 Inhibition Effects.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Lipophilic Constituents inFrontiers in pharmacology · 2022Article
- Target identification of hepatic fibrosis using Pien Tze Huang based on mRNA and lncRNA.Scientific reports · 2021Article
- Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus.Translational neuroscience · 2020Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CCM111 is an aqueous extract of Antrodia cinnamomea (AC) that has exhibited anti-liver fibrosis functions. However, the detailed mechanisms of AC action against liver fibrosis have not been elucidated yet. The present research showed that CCM111 significantly lowered the levels of the hepatic enzyme markers glutamate oxaloacetate transaminase (GOT) and glutamic pyruvic transaminase (GPT), prevented liver damage and collagen deposition, and downregulated TGF-β/Smad signaling in a dose-dependent manner compared with CCl
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Registered trials
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