Liu Ting, Zhou Yu, Ko Kwang Suk, Yang Heping
Department of Gastroenterology, Xiangya Hospital Central South University, 87 Xiangya Road, Changsha, Hunan 410008, China.
GI Liver Center, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Mediators Inflamm. 2015;2015:276850. doi: 10.1155/2015/276850. Epub 2015 Oct 5.
Most chronic liver diseases (CLDs) are characterized by inflammatory processes with aberrant expressions of various pro- and anti-inflammatory mediators in the liver. These mediators are the driving force of many inflammatory liver disorders, which often result in fibrosis, cirrhosis, and liver tumorigenesis. c-Myc is involved in many cellular events such as cell growth, proliferation, and differentiation. c-Myc upregulates IL-8, IL-10, TNF-α, and TGF-β, while IL-1, IL-2, IL-4, TNF-α, and TGF-β promote c-Myc expression. Their interactions play a central role in fibrosis, cirrhosis, and liver cancer. Molecular interference of their interactions offers possible therapeutic potential for CLDs. In this review, current knowledge of the molecular interactions between c-Myc and various well known inflammatory mediators is discussed.
大多数慢性肝病（CLDs）的特征是肝脏中存在炎症过程，伴有各种促炎和抗炎介质的异常表达。这些介质是许多炎症性肝病的驱动力，常导致纤维化、肝硬化和肝脏肿瘤发生。c-Myc参与许多细胞活动，如细胞生长、增殖和分化。c-Myc上调白细胞介素-8（IL-8）、白细胞介素-10（IL-10）、肿瘤坏死因子-α（TNF-α）和转化生长因子-β（TGF-β），而白细胞介素-1（IL-1）、白细胞介素-2（IL-2）、白细胞介素-4（IL-4）、肿瘤坏死因子-α和转化生长因子-β促进c-Myc表达。它们之间的相互作用在纤维化、肝硬化和肝癌中起核心作用。对它们相互作用的分子干扰为慢性肝病提供了潜在的治疗可能性。在本综述中，讨论了目前关于c-Myc与各种知名炎症介质之间分子相互作用的知识。
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