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留学生生物医学工程论文写作文献-Liver Regeneration

Liver Regeneration
Nelson Fausto,1 Jean S. Campbell,1 and Kimberly J. Riehle1,2
During liver regeneration after partial hepatectomy, normally quiescent hepatocytes undergoone or two rounds of replication to restore the liver mass by a process of compensatoryhyperplasia. A large number of genes are involved in liver regeneration, but the essentialcircuitry required for the process may be categorized into three networks: cytokine, growthfactor and metabolic. There is much redundancy within each network, and intricate interactionsexist between them. Thus, loss of function from a single gene rarely leads to completeblockage of liver regeneration. The innate immune system plays an important role in theinitiation of liver regeneration after partial hepatectomy, and new cytokines and receptorsthat participate in initiation mechanisms have been identified. Hepatocytes primed by theseagents readily respond to growth factors and enter the cell cycle. Presumably, the increasedmetabolic demands placed on hepatocytes of the regenerating liver are linked to the machineryneeded for hepatocyte replication, and may function as a sensor that calibrates theregenerative response according to body demands. In contrast to the regenerative processafter partial hepatectomy, which is driven by the replication of existing hepatocytes, liver
repopulation after acute liver failure depends on the differentiation of progenitor cells. Suchcells are also present in chronic liver diseases, but their contribution to the production ofhepatocytes in those conditions is unknown. Most of the new knowledge about the molecularand cellular mechanisms of liver regeneration is both conceptually important anddirectly relevant to clinical problems. (HEPATOLOGY 2006;43:S45-S53.)
The evolution of ideas pertaining to the mechanismsof liver regeneration may be categorizedinto three phases: (1) the original view that a singlehumoral agent could function as a key, capable of
unlocking all of the events required for liver regeneration;
(2) the idea that the activation of one pathway involvingmultiple components could be responsible for regeneration;and (3) the more recent idea that the activity ofmultiple pathways is required for liver regeneration.1-3
This last formulation is still an oversimplification of amore complex reality, as liver regeneration does require
the activation of multiple pathways, but these pathways
do not act independently of each other. The patterns of
interaction between pathways are particularly complex
because they may involve simultaneous and/or sequential
modes of operation, may occur in different liver cell types,
and may be present only at certain stages of liver regeneration.
The recent literature is replete with data showing that
the ablation of genes involved in different pathways can
inhibit liver regeneration, leading to the notion that this
process requires the activation of dozens of different pathways.
An alternative view, which we propose, is that the



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