Evidence map›Paper›PMID 40528724›Full record

ArticleHistology and histopathology2026

PU.1 aggravates hepatic sinusoidal obstruction syndrome by upregulating PTBP1 and activating the Wnt/β-catenin pathway.

Li Yang, Honglin Ju, Zhiyuan Chen, Siqi Cheng, Ya Liu, Xiangyang Wang

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Article in Histology and histopathology, 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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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Li YangDepartment of Gastroenterology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, PR China. xyfeyl@163.com.
Honglin JuDepartment of Gastroenterology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, PR China.
Zhiyuan ChenDepartment of Gastroenterology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, PR China.
Siqi ChengDepartment of Gastroenterology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, PR China.
Ya LiuDepartment of Gastroenterology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, PR China.
Xiangyang WangDepartment of Gastroenterology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, PR China. wangxiangyang@hunnu.edu.cn.

Funding

Research on the Mechanism of PU.1 Transcriptionally Regulating miR-511-3p to Activate the Wnt/β-catenin Signaling Pathway in Hepatic Sinusoidal Obstruction Syndrome 2022JJ30344
6 · The paper itself

Abstract

objectiveHepatic sinusoidal obstruction syndrome (HSOS) is a disease characterized by damage to hepatic sinusoidal endothelial cells (HSECs). This research investigates the role and regulatory pathway of PU box-binding protein (PU.1) in the progression of HSOS.

methodsWe established an

resultsPU.1 was upregulated in MCT-induced HSOS, contributing to elevated oxidative stress and activation of the Wnt/β-catenin pathway. PU.1 directly enhanced PTBP1 transcription, which stabilized β-catenin mRNA and sustained Wnt/β-catenin signaling. PU.1 knockdown alleviated oxidative stress, reduced liver damage, and disrupted the PTBP1-β-catenin interaction, leading to Wnt/β-catenin activity inhibition. Overexpression of PTBP1 reversed the protective effects of PU.1 knockdown, reinstating oxidative stress and reactivating Wnt/β-catenin signaling.

conclusionPU.1 facilitated HSOS pathogenesis by promoting the transcriptional activity of PTBP1 and activating the Wnt/β-catenin pathway. Targeting PU.1 can serve as a promising therapeutic strategy for reducing oxidative stress and liver damage in HSOS.

Indexed as

Hepatic Veno-Occlusive DiseaseHeterogeneous-Nuclear RibonucleoproteinsPolypyrimidine Tract-Binding ProteinProto-Oncogene ProteinsTrans-ActivatorsWnt Signaling PathwayAnimalsbeta CateninDisease Models, AnimalEndothelial CellsLiverMaleMiceMice, Inbred C57BLOxidative StressProto-Oncogene Protein Spi-1beta CateninHeterogeneous-Nuclear RibonucleoproteinsPolypyrimidine Tract-Binding ProteinProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Ptbp1 protein, mouseTrans-Activators

Identifiers

PMID40528724

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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.