Abstract
Apoptosis is a prominent characteristic in the pathogenesis of liver disease. The molecular mechanism of hepatic apoptosis is not well understood. Liver injury induces a downregulation of hepatocyte nuclear factor 6 (HNF6) that is negatively correlated with the degree of apoptosis. However, an enhancement of HNF6 can relieve hepatic apoptosis and impede the progression of liver disease. HNF6 has distinct mechanisms to modulate hepatic apoptosis. Pathophysiological role of HNF6 may be apoptosis-resistant and liver-protective during different types of liver injury. The enhancing modality of HNF6 is a novel therapeutic intervention for liver disease.
Keywords: Hepatic apoptosis, HNF6, liver injury, nuclear factor.
Current Molecular Medicine
Title:Pathophysiological Role of Hepatocyte Nuclear Factor 6 in Negative Regulation of Hepatic Apoptosis: A Novel Hypothesis
Volume: 15 Issue: 5
Author(s): K. Wang
Affiliation:
Keywords: Hepatic apoptosis, HNF6, liver injury, nuclear factor.
Abstract: Apoptosis is a prominent characteristic in the pathogenesis of liver disease. The molecular mechanism of hepatic apoptosis is not well understood. Liver injury induces a downregulation of hepatocyte nuclear factor 6 (HNF6) that is negatively correlated with the degree of apoptosis. However, an enhancement of HNF6 can relieve hepatic apoptosis and impede the progression of liver disease. HNF6 has distinct mechanisms to modulate hepatic apoptosis. Pathophysiological role of HNF6 may be apoptosis-resistant and liver-protective during different types of liver injury. The enhancing modality of HNF6 is a novel therapeutic intervention for liver disease.
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Cite this article as:
Wang K., Pathophysiological Role of Hepatocyte Nuclear Factor 6 in Negative Regulation of Hepatic Apoptosis: A Novel Hypothesis, Current Molecular Medicine 2015; 15 (5) . https://dx.doi.org/10.2174/1566524015666150630124142
DOI https://dx.doi.org/10.2174/1566524015666150630124142 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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