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自1972年病理学家Kerr首先提出细胞凋亡的概念以来,其重要的生理意义早为人们所熟知,近年来研究发现细胞凋亡与各种肝病有密切关系,细胞凋亡的基因调控一直是研究热点,现扼要综述肝细胞凋亡基因调控研究进展。 1 诱导和增加细胞凋亡的相关基因 1.1 野生型P53(WTP53)WTP53是种抑癌基因,大量研究表明WtP53可促进细胞凋亡,Bellamy等研究表明WTP53在正常细胞周期中不起作用,只在肝细胞受到应激而使DNA损伤时,如营养支持条件减少或受到外源性的肝脏有丝分裂原刺激时,WTP53会发挥分子警察作用,如果此时WTP53缺乏,肝细胞会出现较强的增殖反应,这和肝细胞癌形成有相似的背景,因为肝癌常发生于肝炎和肝硬化的基础上,而且俩者都存在慢性肝细胞破坏,所以WTP53缺乏在慢性肝炎中有利于肝癌的形成。而且HBV X
Since the concept of apoptosis was first proposed by pathologist Kerr in 1972, its important physiological significance has long been known. In recent years, it has been found that apoptosis is closely related to various liver diseases. The gene regulation of apoptosis has been Research hot spots, now summarize the progress of hepatocyte apoptosis gene regulation research. 1 Inducible and Increased Apoptotic Related Genes 1.1 Wild-type P53 (WTP53) WTP53 is a tumor suppressor gene. A large number of studies have shown that WtP53 can promote apoptosis. Bellamy et al. Showed that WTP53 does not play a role in normal cell cycle, WTP53 will play a role of molecular police when hepatocytes are damaged by DNA damage, such as reduced nutritional support or exogenous liver mitogen stimulation. If WTP53 is deficient at this moment, hepatocytes will have a strong proliferative response , Which is similar to the formation of hepatocellular carcinoma. Because liver cancer often occurs on the basis of hepatitis and cirrhosis, and both have chronic hepatocellular destruction, the lack of WTP53 contributes to the formation of liver cancer in chronic hepatitis. And HBV X.