Department of General Surgery, Hokkaido University School of Medicine, N-15, W-7 Kita-ku, Sapporo, Hokkaido 060-8638, Japan.
J Hepatobiliary Pancreat Sci. 2011 Jan;18(1):13-22. doi: 10.1007/s00534-010-0304-2.
Liver regeneration is a necessary process that most liver damage depends on for recovery. Regeneration is achieved by a complex interactive network consisting of liver cells (hepatocytes, Kupffer cells, sinusoidal endothelial cells, hepatic stellate cells, and stem cells) and extrahepatic organs (thyroid gland, adrenal gland, pancreas, duodenum, and autonomous nervous system). The restoration of liver volume depends on hepatocyte proliferation, which includes initiation, proliferation, and termination phases. Hepatocytes are "primed" mainly by Kupffer cells via cytokines (IL-6 and TNF-alpha) and then "proliferation" and "cell growth" of hepatocytes are induced by the stimulations of cytokines and growth factors (HGF and TGF-alpha). Liver regeneration is achieved by cell proliferation and cell growth, where the IL-6/STAT3 and PI3-K/PDK1/Akt pathways play pivotal roles, respectively. IL-6/STAT3 pathway regulates hepatocyte proliferation via cyclin D1/p21 and protects against cell death by upregulating FLIP, Bcl-2, Bcl-xL, Ref1, and MnSOD. PI3-K/PDK1/Akt is known to be responsible for regulation of cell size via its downstream molecules such as mTOR in addition to being known for its survival, anti-apoptotic and anti-oxidative properties. Although the molecular mechanisms of liver regeneration have been actively studied, the mechanisms of liver regeneration must be elucidated and leveraged for the sufficient treatment of liver diseases.
肝脏再生是一种必要的过程,大多数肝脏损伤都依赖于这种过程来恢复。再生是通过一个由肝脏细胞(肝细胞、库普弗细胞、肝窦内皮细胞、肝星状细胞和干细胞)和肝外器官(甲状腺、肾上腺、胰腺、十二指肠和自主神经系统)组成的复杂交互网络来实现的。肝脏体积的恢复取决于肝细胞的增殖,包括起始、增殖和终止阶段。肝细胞主要通过库普弗细胞通过细胞因子(IL-6 和 TNF-alpha)“启动”,然后通过细胞因子和生长因子(HGF 和 TGF-alpha)的刺激诱导肝细胞的“增殖”和“细胞生长”。肝脏再生是通过细胞增殖和细胞生长来实现的,其中 IL-6/STAT3 和 PI3-K/PDK1/Akt 途径分别发挥关键作用。IL-6/STAT3 途径通过细胞周期蛋白 D1/p21 调节肝细胞增殖,并通过上调 FLIP、Bcl-2、Bcl-xL、Ref1 和 MnSOD 来防止细胞死亡。PI3-K/PDK1/Akt 除了具有生存、抗凋亡和抗氧化特性外,还被认为负责通过其下游分子如 mTOR 来调节细胞大小。尽管肝脏再生的分子机制已经得到了积极的研究,但必须阐明肝脏再生的机制,并利用这些机制充分治疗肝脏疾病。