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Journal of Zhejiang University SCIENCE B
ISSN 1673-1581(Print), 1862-1783(Online), Monthly
2024 Vol.25 No.6 P.451-470
Key role of interferon regulatory factor 1 (IRF-1) in regulating liver disease: progress and outlook
Abstract: Interferon regulatory factor 1 (IRF-1) is a member of the IRF family. It is the first transcription factor to be identified that could bind to the interferon-stimulated response element (ISRE) on the target gene and displays crucial roles in the interferon-induced signals and pathways. IRF-1, as an important medium, has all of the advantages of full cell cycle regulation, cell death signaling transduction, and reinforcing immune surveillance, which are well documented. Current studies indicate that IRF-1 is of vital importance to the occurrence and evolution of multifarious liver diseases, including but not limited to inhibiting the replication of the hepatitis virus (A/B/C/E), alleviating the progression of liver fibrosis, and aggravating hepatic ischemia-reperfusion injury (HIRI). The tumor suppression of IRF-1 is related to the clinical characteristics of liver cancer patients, which makes it a potential indicator for predicting the prognosis and recurrence of liver cancer; additionally, the latest studies have revealed other effects of IRF-1 such as protection against alcoholic/non-alcoholic fatty liver disease (AFLD/NAFLD), cholangiocarcinoma suppression, and uncommon traits in other liver diseases that had previously received little attention. Intriguingly, several compounds and drugs have featured a protective function in specific liver disease models in which there is significant involvement of the IRF-1 signal. In this paper, we hope to propose a prospective research basis upon which to help decipher translational medicine applications of IRF-1 in liver disease treatment.
Key words: Interferon regulatory factor (IRF-1); Hepatitis virus; Liver fibrosis; Hepatic ischemia-reperfusion injury (HIRI); Liver cancer
机构:1合肥工业大学,土木与水利工程学院,中国合肥,230009;2中国矿业大学,力学与土木工程学院,中国徐州,221116
目的:岩石宏观变形破坏演化特征受其内部初始微裂纹的影响,但在理论计算、数值模拟和力学实验中,这部分影响往往被忽略。本文旨在提出一个定量分析模型来研究初始微裂纹对岩石变形破坏演化过程的影响。
创新点:1.建立初始微裂纹占比定量分析的理论模型;2.揭示围压对大理岩模型参数演化的影响。
方法:1.通过理论推导,建立一种能进行岩石初始微裂纹占比定量分析的理论模型,并基于三轴压缩试样的应力分解改进该模型的表达式(公式(13)和(14));2.通过三轴压缩试验,确定岩石初始裂隙精确分析的拟合区间,并分析围压对大理岩试样模型参数演化的影响(图5~7);3.结合微CT扫描技术,对受载岩样的裂隙演化特征进行讨论与分析(图10和11)。
结论:1.所建立的岩石初始微裂纹占比定量分析模型参数物理意义明确、确定方便;2.随着围压的增加,试样孔隙度和泊松比均以指数函数的形式递减,基质部分弹性模量先增大后趋于稳定,而微裂纹弹性模量呈指数增长;3.试样破坏是试样内部微裂纹扩展的结果,且宏观破坏角随着围压的增大而线性减小。
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DOI:
10.1631/jzus.B2300159
CLC number:
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On-line Access:
2024-08-27
Received:
2023-10-17
Revision Accepted:
2024-05-08
Crosschecked:
2024-06-24