Evidence map›Paper›PMID 33609067›Full record

ArticleJournal of cellular and molecular medicine2021

Lenvatinib prevents liver fibrosis by inhibiting hepatic stellate cell activation and sinusoidal capillarization in experimental liver fibrosis.

Hiroyuki Ogawa, Kosuke Kaji, Norihisa Nishimura, Hirotetsu Takagi, Koji Ishida, Hiroaki Takaya, Hideto Kawaratani, Kei Moriya, Tadashi Namisaki, Takemi Akahane and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 14% of its field
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

11 citing papers in PubMed, 19 citations in OpenAlex.

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  6. [Chinese expert guidance on overall application of lenvatinib in hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023
    Article
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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

11 authors at 1 institution in 1 country.

Hiroyuki OgawaDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Kosuke KajiDepartment of Gastroenterology, Nara Medical University, Nara, Japan.ORCID 0000-0002-1822-6759
Norihisa NishimuraDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Hirotetsu TakagiDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Koji IshidaDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Hiroaki TakayaDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Hideto KawarataniDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Kei MoriyaDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Tadashi NamisakiDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Takemi AkahaneDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Hitoshi YoshijiDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Nara Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular targeted agents are pharmacologically used to treat liver fibrosis and have gained increased attention. The present study examined the preventive effect of lenvatinib on experimental liver fibrosis and sinusoidal capillarization as well as the in vitro phenotypes of hepatic stellate cells. LX-2, a human stellate cell line, was used for in vitro studies. In vivo liver fibrosis was induced in F344 rats using carbon tetrachloride by intraperitoneal injection for 8 weeks, and oral administration of lenvatinib was started two weeks after initial injection of carbon tetrachloride. Lenvatinib restrained proliferation and promoted apoptosis of LX-2 with suppressed phosphorylation of extracellular signal-regulated kinase 1/2 and AKT. It also down-regulated COL1A1, ACTA2 and TGFB1 expressions by inhibiting the transforming growth factor-β1/Smad2/3 pathway. Treatment with lenvatinib also suppressed platelet-derived growth factor-BB-stimulated proliferation, chemotaxis and vascular endothelial growth factor-A production, as well as basic fibroblast growth factor-induced LX-2 proliferation. In vivo study showed that lenvatinib attenuated liver fibrosis development with reduction in activated hepatic stellate cells and mRNA expression of profibrogenic markers. Intrahepatic neovascularization was ameliorated with reduced hepatic expressions of Vegf1, Vegf2 and Vegfa in lenvatinib-treated rats. Collectively, these results suggest the potential use of lenvatinib as a novel therapeutic strategy for liver fibrosis.

Indexed as

AnimalsCapillariesCarbon TetrachlorideCells, CulturedHepatic Stellate CellsLiverLiver CirrhosisMaleNeovascularization, PathologicPhenylurea CompoundsProtein Kinase InhibitorsQuinolinesRatsRats, Inbred F344Carbon TetrachloridelenvatinibPhenylurea CompoundsProtein Kinase InhibitorsQuinolinesangiogenesishepatic stellate celllenvatinibliver fibrosisPDGFVEGF

Identifiers

PMID33609067
PMCPMC8051749
OpenAlexW3131764533

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.