The adult liver exhibits the remarkable ability to “regenerate” following surgical resection or toxic liver injuries. Restoration of the hepatic tissue occurs through rapid proliferation of adult mature hepatocytes. The hepatocytes expressing the liver-specific functions are quiescent cells that keep the ability to reenter the cell cycle. The fact that liver regeneration is supported by the active proliferation of differentiated hepatocytes rather than the expansion of progenitor cells is a unique situation among adult solid tissues. The entry into and progression through G1 phase of the cell cycle are orchestrated by complex networks of extracellular stimuli and intracellular signaling pathways, inducing profound modifications of the gene expression profile required for the switch from quiescence to proliferation. Several lines of evidences also indicate that cell cycle regulators such as the cyclin-dependent protein kinases (CDKs) and their functional partners, the cyclins and CDK inhibitors (CDKIs), show specific expression and/or activation patterns compared to the cell cycle in other cell types. In addition, polyploidy is another characteristic feature of mammalian adult hepatocytes that contributes to the specific regulation of the cell cycle in hepatocytes. We invite authors to submit original research as well as review articles that will contribute to further defining the cellular and molecular mechanisms underlying the cell cycle regulation of the adult hepatocytes.

We are more particularly interested in articles that explore the signaling pathways and the cell cycle protein kinases, controlling the proliferation of adult hepatocytes during liver regeneration in vivo or in in vitro cell models. Potential topics include, but are not limited to:

• Liver microenvironment and initiation of liver regeneration (priming)
• Intracellular signaling pathways and gene profile modifications controlling the priming and progression in early G1 phase of the cell cycle
• Molecular mechanisms and protein kinases controlling the G1/S and G2/M transitions
• Hepatic polyploidy status and cell cycle
• Extra- and intracellular signaling pathways regulating the hepatocyte cell cycle arrest

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/ijhep/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable: