| pubmed-article:21326550 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21326550 | lifeskim:mentions | umls-concept:C0023907 | lld:lifeskim |
| pubmed-article:21326550 | lifeskim:mentions | umls-concept:C0439855 | lld:lifeskim |
| pubmed-article:21326550 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:21326550 | pubmed:dateCreated | 2011-2-17 | lld:pubmed |
| pubmed-article:21326550 | pubmed:abstractText | The atrophy-hypertrophy complex (AHC) refers to the controlled restoration of liver parenchyma following hepatocyte loss. Different types of injury (e.g., toxins, ischemia/reperfusion, biliary obstruction, and resection) elicit the same hypertrophic response in the remnant liver. The AHC involves complex anatomical, histological, cellular, and molecular processes. The signals responsible for these processes are both intrinsic and extrinsic to the liver and involve both physical and molecular events. In patients in whom resection of large liver malignancies would result in an inadequate functional liver remnant, preoperative portal vein embolization may increase the remnant liver sufficiently to permit aggressive resections. Through continued basic science research, the cellular mechanisms of the AHC may be maximized to permit curative resections in patients with potentially prohibitive liver function. | lld:pubmed |
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