Evidence map›Paper›PMID 40326028›Full record

ArticleCurrent medicinal chemistry2026

Icaritin Attenuates HSC Activation by Down-regulating the HIF-1α and TGF-β/Smad Signaling Pathways to Ameliorate Liver Fibrosis.

Keping Feng, Qiaoman Fei, Na Huang, Ke Du, Chengbo Zhang, Yudan Fan, Ying Zhou, Yaping Zhao, Pengfei Liu, Zongfang Li

Abstract read
In one paragraph

Article in Current medicinal chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Keping FengNational-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
Qiaoman FeiNational-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
Na HuangNational-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
Ke DuNational-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
Chengbo ZhangNational-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
Yudan FanNational-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
Ying ZhouShaanxi International Cooperation Base for Inflammation and Immunity, Xi'an, 710004, China.
Yaping ZhaoNational-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
Pengfei LiuNational-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
Zongfang LiNational-Local Joint Engineering Research Center of Biodiagnostic & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.

Funding

Basic-Clinical Integration program of Xi'an Jiaotong University YXJLRH2022064National Natural Science Foundation of China 82003905Natural Science Foundation of Shaanxi Province 2019JQ-963, 2020JQ-541
6 · The paper itself

Abstract

introductionIcaritin is a bioactive flavonol isolated from the Chinese medicinal herb Epimedium. The comprehensive understanding of antifibrotic effects and associated molecular mechanisms of icaritin remains incomplete. This study aims to explore the protective effects of icaritin against liver fibrosis and to further elucidate the mechanisms involved.

methodsHuman hepatic stellate LX-2 cells stimulated with TGF-β1 and a carbon tetrachloride (CCl4)-induced liver fibrosis mouse model were employed. In vitro assays were carried out to evaluate collagen type I (COL I) and α-smooth muscle actin (α-SMA) expression, while in vivo studies assessed fibrosis alleviation. Molecular mechanisms were explored via analysis of TGF-β1, phosphorylated Smad2/3, and HIF-1α protein levels using Western blotting.

resultsIcaritin suppressed TGF-β1-induced COL I and α-SMA expression in LX-2 cells and ameliorated liver fibrosis in CCl4-treated mice. Mechanistically, it significantly reduced TGF-β1 levels, inhibited Smad2/3 phosphorylation, and downregulated HIF-1α protein expression in LX-2 cells.

conclusionIcaritin attenuated experimental liver fibrosis through the inhibition of the TGF-β/Smad and HIF-1α signaling pathways, highlighting its therapeutic potential for fibrotic liver diseases.

Indexed as

Down-RegulationFlavonoidsHepatic Stellate CellsHypoxia-Inducible Factor 1, alpha SubunitLiver CirrhosisSignal TransductionSmad ProteinsTransforming Growth Factor betaAnimalsCarbon TetrachlorideCell LineHumansMaleMiceMice, Inbred C57BLTransforming Growth Factor beta1Carbon TetrachlorideFlavonoidsHypoxia-Inducible Factor 1, alpha SubuniticaritinSmad ProteinsTransforming Growth Factor betaTransforming Growth Factor beta1antifibrotic therapyhepatic stellate cell (HSC) activationHIF-1αIcaritinliver fibrosisTGF-β/Smad

Identifiers

PMID40326028
PMCPMC13555768

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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.