Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis-C-virus-related infective diseases are worldwide spread pathologies affecting primarily liver. The infection is often asymptomatic, but when chronically persisting can lead to liver scarring and ultimately to cirrhosis, which is generally apparent after decades. In some cases, cirrhosis will progress to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices. HCV-infected cells undergo profound metabolic dysregulation whose mechanisms are yet not well understood. An emerging feature in the pathogenesis of the HCV-related disease is the setting of a pro-oxidative condition caused by dysfunctions of mitochondria which proved to be targets of viral proteins. This causes deregulation of mitochondria-dependent catabolic pathway including fatty acid oxidation. Nuclear receptors and their ligands are fundamental regulators of the liver metabolic homeostasis, which are disrupted following HCV infection. In this contest, specific attention has been focused on the peroxisome proliferator activated receptors given their role in controlling liver lipid metabolism and the availability of specific pharmacological drugs of potential therapeutic utilization. However, the reported role of PPARs in HCV infection provides conflicting results likely due to different species-specific contests. In this paper we summarize the current knowledge on this issue and offer a reconciling model based on mitochondria-related features.
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PMID:PPARs and HCV-Related Hepatocarcinoma: A Mitochondrial Point of View. 2296 21

The liver has a unique and extraordinary capacity for regeneration, even in adult organisms. This regenerative potential has traditionally been attributed to the replicative capabilities of mature hepatocytes and cholangiocytes, though emerging evidence suggests that other resident liver cell types such as progenitors, liver sinusoidal endothelial cells, and hepatic stellate cells respond to liver injury and contribute to repair. These other cells types are also associated with liver scarring, dysfunction, and carcinogenesis, which suggests that appropriate regulation of these cells is a major determinant of response to liver injury. The Reviews in this series explore possible contributions of liver progenitor cells, liver sinusoidal endothelial cells, and hepatic stellate cells to liver homeostasis and repair and highlight how these processes can go awry in chronic liver injury, fibrosis, and liver cancer.
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PMID:Underlying potential: cellular and molecular determinants of adult liver repair. 2363 82