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Vitamin D ‐ liver disease association: Biological basis and mechanisms of action
Christos Triantos
Ioanna Aggeletopoulou
Konstantinos Thomopoulos
Athanasia Mouzaki
First published: 06 January 2021
https://doi.org/10.1002/hep.31699
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi:10.1002/hep.31699
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Abstract
Vitamin D plays a major role in hepatic pathophysiology, demonstrated by studies showing that it actively inhibits liver fibrosis and that its deficiency is associated with liver dysfunction and severity of liver diseases. Vitamin D and its receptor (VDR) are involved in the regulation of innate and adaptive immune responses and emerging evidence suggests that they contribute to liver homeostasis by exerting antiproliferative, anti‐inflammatory and antifibrotic activities. Over the last decades, extensive research has been focused on the identification of the biochemical and molecular pathways that mediate vitamin D‐VDR cellular and genomic actions through which vitamin D regulates the expression of target genes and modulates the progression of liver diseases. In this review, we discuss the recent advances in our understanding of the molecular mechanisms involved in vitamin D‐VDR signaling and how genetic variants influence inflammatory responses and fibrogenic outcomes. The delineation of the biological basis of the association between vitamin D and liver disease progression is important for the development of novel treatment strategies for liver diseases.
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发表于 2021-1-16 13:35
