Wnt/β-Catenin Signaling in Liver Pathobiology

IF 28.4 1区 医学 Q1 PATHOLOGY
Matthew D. Carson, Kari Nejak-Bowen
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引用次数: 0

Abstract

The liver has a critical role in regulating host metabolism, immunity, detoxification, and homeostasis. Proper liver function is essential for host health, and dysregulation of hepatic signaling pathways can lead to the onset of disease. The Wnt/β-catenin signaling pathway is an important regulator of liver homeostasis and function. Throughout life, hepatic Wnt/β-catenin signaling contributes to liver development and growth, metabolic zonation, and regeneration. Extensive research has demonstrated that aberrant Wnt/β-catenin signaling drives liver pathologies, including cancers, steatohepatitis, and cholestasis. In this review, we discuss the Wnt/β-catenin pathway as it pertains to liver function and how disruptions in this pathway contribute to the onset and progression of liver diseases. Further, we discuss ongoing research that targets the Wnt/β-catenin pathway for the treatment of liver pathologies.
肝脏病理生物学中的 Wnt/β-Catenin 信号转导
肝脏在调节宿主新陈代谢、免疫、解毒和体内平衡方面起着至关重要的作用。肝脏的正常功能对宿主的健康至关重要,而肝脏信号通路的失调可导致疾病的发生。Wnt/β-catenin信号通路是肝脏稳态和功能的重要调节因子。在人的一生中,肝脏 Wnt/β-catenin 信号通路有助于肝脏的发育和生长、代谢分区和再生。大量研究表明,Wnt/β-catenin 信号传导异常会导致肝脏病变,包括癌症、脂肪性肝炎和胆汁淤积。在这篇综述中,我们将讨论与肝功能有关的 Wnt/β-catenin 通路,以及该通路的中断如何导致肝病的发生和发展。此外,我们还讨论了目前针对 Wnt/β-catenin 通路治疗肝脏病变的研究。
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来源期刊
CiteScore
62.60
自引率
0.00%
发文量
40
期刊介绍: The Annual Review of Pathology: Mechanisms of Disease is a scholarly journal that has been published since 2006. Its primary focus is to provide a comprehensive overview of recent advancements in our knowledge of the causes and development of significant human diseases. The journal places particular emphasis on exploring the current and evolving concepts of disease pathogenesis, as well as the molecular genetic and morphological changes associated with various diseases. Additionally, the journal addresses the clinical significance of these findings. In order to increase accessibility and promote the broad dissemination of research, the current volume of the journal has transitioned from a gated subscription model to an open access format. This change has been made possible through the Annual Reviews' Subscribe to Open program, which allows all articles published in this volume to be freely accessible to readers. As part of this transition, all articles in the journal are published under a Creative Commons Attribution (CC BY) license, which encourages open sharing and use of the research.
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