ArticleMolecules (Basel, Switzerland)2019
12N-Substituted Matrinol Derivatives Inhibited the Expression of Fibrogenic Genes via Repressing Integrin/FAK/PI3K/Akt Pathway in Hepatic Stellate Cells.
Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Integrated proteomic and metabolomic analysis reveals the mechanism of astragalus complanatus flavonoids against liver fibrosis in rats.Frontiers in pharmacology · 2026Article
- Ethoxychelerythrine as a potential therapeutic strategy targets PI3K/AKT/mTOR induced mitochondrial apoptosis in the treatment of colorectal cancer.Scientific reports · 2025Article
- Recent advances in the role of polysaccharides in liver diseases: a review.Frontiers in pharmacology · 2025Review
- The effect of saraglitazar on TGF-β-induced smad3 phosphorylation and expression of genes related to liver fibrosis in LX2 cell line.Molecular biology reports · 2024Article
- Discovery of 9O-Substituted Palmatine Derivatives as a New Class of anti-COL1A1 Agents via Repressing TGF-β1/Smads and JAK1/STAT3 Pathways.Molecules (Basel, Switzerland) · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Twenty new 12N-substituted matrinol derivatives were synthesized and evaluated for their inhibitory effects on collagen α1 (I) (COL1A1) promotor in human hepatic stellate LX-2 cells. The structure-activity relationship (SAR) revealed that introducing a 12N-benzeneaminoacylmethyl substitution might significantly enhance the activity. Compound 8a exhibited the highest inhibitory potency against COL1A1, and its inhibition activity against COL1A1 was further confirmed on both the mRNA and protein levels. It also effectively inhibited the expression of α smooth muscle actin (α-SMA), fibronectin and transforming growth factor β1 (TGFβ1), indicating an extensive inhibitory effect on the expression of fibrogenic genes. The primary mechanism study indicated that it might take action via the Integrin/FAK/PI3K/Akt signaling pathway. The results provided powerful information for further structure optimization, and compound 8a was selected as a novel anti-fibrogenic lead for further investigation.
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Registered trials
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