Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.
Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri; Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri.
Am J Pathol. 2014 Feb;184(2):309-21. doi: 10.1016/j.ajpath.2013.04.034. Epub 2013 Oct 17.
The regenerative capability of liver is well known, and the mechanisms that regulate liver regeneration are extensively studied. Such analyses have defined general principles that govern the hepatic regenerative response and implicated specific extracellular and intracellular signals as regulated during and essential for normal liver regeneration. Nevertheless, the most proximal events that stimulate liver regeneration and the distal signals that terminate this process remain incompletely understood. Recent data suggest that the metabolic response to hepatic insufficiency might be the proximal signal that initiates regenerative hepatocellular proliferation. This review provides an overview of the data in support of a metabolic model of liver regeneration and reflects on the clinical implications and areas for further study suggested by these findings.
肝脏的再生能力是众所周知的，调节肝脏再生的机制也得到了广泛的研究。这些分析定义了指导肝再生反应的一般原则，并表明特定的细胞外和细胞内信号在正常肝再生过程中受到调节，对其是必不可少的。然而，刺激肝再生的最近端事件和终止这一过程的远端信号仍不完全清楚。最近的数据表明，肝脏功能不全的代谢反应可能是启动再生肝细胞增殖的近端信号。这篇综述概述了支持肝脏再生代谢模型的数据，并对这些发现所提示的临床意义和进一步研究领域进行了思考。
