期刊
SEMINARS IN LIVER DISEASE
卷 37, 期 2, 页码 141-151出版社
THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0037-1601351
关键词
partial hepatectomy; cellular and molecular basis; hepatocyte proliferation; inflammation; stellate cells; endothelial cells; initiation; signaling pathways; hepatocytes; nonparenchymal cells
资金
- NIH [R01DK62277, R01DK100287, R01DK095498, R01CA204586]
- Endowed Chair for Experimental Pathology
Liver possesses many critical functions such as synthesis, detoxification, and metabolism. It continually receives nutrient-rich blood from gut, which incidentally is also toxin-rich. That may be why liver is uniquely bestowed with a capacity to regenerate. A commonly studied procedure to understand the cellular and molecular basis of liver regeneration is that of surgical resection. Removal of two-thirds of the liver in rodents or patients instigates alterations in hepatic homeostasis, which are sensed by the deficient organ to drive the restoration process. Although the exact mechanisms that initiate regeneration are unknown, alterations in hemodynamics and metabolism have been suspected as important effectors. Key signaling pathways are activated that drive cell proliferation in various hepatic cell types through autocrine and paracrine mechanisms. Once the prehepatectomy mass is regained, the process of regeneration is adequately terminated. This review highlights recent discoveries in the cellular and molecular basis of liver regeneration.
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