Evidence map›Paper›PMID 42414677›Full record

ArticleActa parasitologica2026

Effect of LY2109761 on TGF-β1/TGFβRI/Smad Pathway and Hepatic Fibrosis Cysts Formation in Rats Infected with Echinococcus granulosus: an In Vitro and In Vivo Study.

Shaohua Zhai, Yueqi Yang, Meihe Hu, Yang Zhou, Yanshuang Yang, Nijun Zou

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Article in Acta parasitologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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6 authors.

Shaohua Zhai *College of Veterinary Medicine, Xinjiang Agricultural University, Ürümqi, 830052, China. 18309916937@163.com.
Yueqi Yang *College of Veterinary Medicine, Xinjiang Agricultural University, Ürümqi, 830052, China.
Meihe HuYili Chuanning Biotechnology Co., Ltd., Yili, 835000, China.
Yang ZhouCollege of Veterinary Medicine, Xinjiang Agricultural University, Ürümqi, 830052, China.
Yanshuang YangCollege of Veterinary Medicine, Xinjiang Agricultural University, Ürümqi, 830052, China.
Nijun ZouCollege of Veterinary Medicine, Xinjiang Agricultural University, Ürümqi, 830052, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeEchinococcus granulosus infection is a zoonotic parasite disease that threatens animal husbandry development and farmer and herder health. Hepatic fibrosis cysts induced by protoscoleces (PSCs) are a common pathological alteration. The formation of these cysts is related to the stimulation of TGF-β1/TGFβRI/Smad signaling in hepatic stellate cells (HSCs). TGF-β1 activates the TGFβRI/Smad pathway in HSCs, which is needed in the formation of fibrosis cysts.

methodsLY2109761, a TGF-β receptor inhibitor, is hypothesized to reduce the formation of hepatic fibrosis cysts by limiting TGF-β1 binding to TGFβRI receptors on HSCs and decreasing the activation of the TGFβRI/Smad pathway. Herein, a liver infection model in rats with PSCs was constructed, and the infected rats were treated with LY2109761 in vivo. The pathological morphology, serum IL-1β, IL-2, IL-4, IL5, IL-6, IL-10, IL-13, IL-17 concentrations, TGF-β1 cytokine, and fibrosis TGF-β1/Smad pathway protein expression were detected to verify the mechanism how PSCs infection activates the HSC TGF-β1/ Smad pathway to promote liver fibrosis.

resultsThe study examined how LY2109761 affected TGF-β1 secretion in hepatocytes co-cultured with PSCs and BRL cells in vitro, and the activation of the TGF-β1/Smad in HSC-T6 cells induced by the co-culture supernatant, which ultimately led to liver fibrosis. Prolonged infection duration raised blood concentrations of IL-1β, IL-2, IL-4, IL5,IL-6, IL-10, and IL-17 as well as hepatocyte TGF-β1 production and secretion.

conclusionTGF-β1 acts on HSC surface, where it binds to TGF-βRI to stimulate the production of hepatic fibrosis cysts via TGF-β1/TGFβRI/Smad. Blocking TGF-β1 linking to the TGFβRI receptor can lessen PSCs damage to liver cells, prevent fibrotic cyst formation, and activate the immune system in the body to kill invaders.

Indexed as

EchinococcosisEchinococcus granulosusLiver CirrhosisPyrazolesPyrrolesReceptor, Transforming Growth Factor-beta Type ISignal TransductionSmad ProteinsTransforming Growth Factor beta1AnimalsDisease Models, AnimalHepatic Stellate CellsLiverMaleRatsRats, Sprague-DawleyLY2109761PyrazolesPyrrolesReceptor, Transforming Growth Factor-beta Type ISmad ProteinsTransforming Growth Factor beta1Cyst fibrosisEchinococcus granulosusTGF-β1TGF-β1/TGFβRI/Smad signaling pathway

Identifiers

PMID42414677
PMCPMC13342423

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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.