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孕烷 X 受体信号通路与维生素 K:在人类健康中的分子机制和临床相关性。

Pregnane X Receptor Signaling Pathway and Vitamin K: Molecular Mechanisms and Clinical Relevance in Human Health.

机构信息

Division of Basic Sciences, Farber-McIntire Campus, College of Osteopathic Medicine, Kansas City University, Joplin Campus, 2901 St Johns Blvd, Joplin, MO 64804, USA.

出版信息

Cells. 2024 Apr 14;13(8):681. doi: 10.3390/cells13080681.

DOI:10.3390/cells13080681
PMID:38667296
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11049418/
Abstract

This review explores the likely clinical impact of Pregnane X Receptor (PXR) activation by vitamin K on human health. PXR, initially recognized as a master regulator of xenobiotic metabolism in liver, emerges as a key regulator influencing intestinal homeostasis, inflammation, oxidative stress, and autophagy. The activation of PXR by vitamin K highlights its role as a potent endogenous and local agonist with diverse clinical implications. Recent research suggests that the vitamin K-mediated activation of PXR highlights this vitamin's potential in addressing pathophysiological conditions by promoting hepatic detoxification, fortifying gut barrier integrity, and controlling pro-inflammatory and apoptotic pathways. PXR activation by vitamin K provides an intricate association with cancer cell survival, particularly in colorectal and liver cancers, to provide new insights into potential novel therapeutic strategies. Understanding the clinical implications of PXR activation by vitamin K bridges molecular mechanisms with health outcomes, further offering personalized therapeutic approaches for complex diseases.

摘要

这篇综述探讨了维生素 K 对 PXR(孕烷 X 受体)的激活对人类健康可能产生的临床影响。PXR 最初被认为是肝脏中外源物质代谢的主要调节剂,现已成为影响肠道内稳态、炎症、氧化应激和自噬的关键调节剂。维生素 K 对 PXR 的激活突出了其作为一种强效内源性和局部激动剂的作用,具有广泛的临床意义。最近的研究表明,维生素 K 介导的 PXR 激活强调了这种维生素在通过促进肝脏解毒、增强肠道屏障完整性以及控制促炎和凋亡途径来解决生理病理状况方面的潜力。维生素 K 对 PXR 的激活与癌细胞的存活密切相关,特别是在结直肠癌和肝癌中,为潜在的新治疗策略提供了新的见解。维生素 K 对 PXR 的激活的临床意义将分子机制与健康结果联系起来,为复杂疾病提供了更个性化的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/f882a28c56f9/cells-13-00681-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/c736ca8c6938/cells-13-00681-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/f1a631117361/cells-13-00681-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/71310b9bcf79/cells-13-00681-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/eb42fd5f9911/cells-13-00681-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/f882a28c56f9/cells-13-00681-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/c736ca8c6938/cells-13-00681-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/f1a631117361/cells-13-00681-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/71310b9bcf79/cells-13-00681-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/eb42fd5f9911/cells-13-00681-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0034/11049418/f882a28c56f9/cells-13-00681-g005.jpg

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