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- W2884328615 endingPage "85" @default.
- W2884328615 startingPage "85" @default.
- W2884328615 abstract "Fibrosis is the main consequence of any kind of chronic liver damage. Coagulation and thrombin generation are crucial in the physiological response to tissue injury; however, the inappropriate and uncontrolled activation of coagulation cascade may lead to fibrosis development due to the involvement of several cellular types and biochemical pathways in response to thrombin generation. In the liver, hepatic stellate cells and sinusoidal endothelial cells orchestrate fibrogenic response to chronic damage. Thrombin interacts with these cytotypes mainly through protease-activated receptors (PARs), which are expressed by endothelium, platelets and hepatic stellate cells. This review focuses on the impact of coagulation in liver fibrogenesis, describes receptors and pathways involved and explores the potential antifibrotic properties of drugs active in hemostasis in studies with cells, animal models of liver damage and humans." @default.
- W2884328615 created "2018-08-03" @default.
- W2884328615 creator A5004779104 @default.
- W2884328615 creator A5056404517 @default.
- W2884328615 creator A5088326019 @default.
- W2884328615 date "2018-07-24" @default.
- W2884328615 modified "2023-10-02" @default.
- W2884328615 title "Coagulation, Microenvironment and Liver Fibrosis" @default.
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