Menjo Masafumi, Ikeda Kyoji, Nakanishi Makoto
Department of Geriatric Research, National Institute for Longevity Sciences, Obu, Aichi, Japan.
J Gastroenterol Hepatol. 1998 Sep;13(S1):S100-S105. doi: 10.1111/jgh.1998.13.s1.100.
The liver serves as a suitable model for studying tissue regeneration. Although various growth factors have been implicated in the promotion of this process, their precise role in liver regeneration remains to be elucidated. Whatever the extracellular signals may be, they all converge on cell cycle regulators in the nucleus, where the sequential activation of cyclin-dependent kinases (Cdk) takes place. The activities of Cdk are regulated positively through their association with cognate cyclins, and negatively via interactions with Cdk inhibitors. In this review article, our recent data as well as results of previous reports on how these cell cycle regulators trigger and/or terminate the process of liver regeneration are summarized. The authors believe that 'knockout' mice, in which specific genes are deleted, will be useful for providing further insight into the positive and negative regulation of liver regeneration.
肝脏是研究组织再生的合适模型。尽管多种生长因子与这一过程的促进有关，但其在肝脏再生中的精确作用仍有待阐明。无论细胞外信号是什么，它们都汇聚于细胞核中的细胞周期调节因子，细胞周期蛋白依赖性激酶（Cdk）在此依次被激活。Cdk的活性通过与同源细胞周期蛋白的结合而得到正向调节，并通过与Cdk抑制剂的相互作用而受到负向调节。在这篇综述文章中，我们总结了近期的数据以及先前关于这些细胞周期调节因子如何触发和/或终止肝脏再生过程的报道结果。作者认为，特定基因被敲除的“基因敲除”小鼠将有助于进一步深入了解肝脏再生的正负调节机制。
