Hepatic Angiogenesis

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Abstract
Angiogenesis is an essential process for organ growth and repair. Thus, an imbalance in this process can lead to several diseases including malignancy. Angiogenesis is a critical step in vascular remodeling, tissue damage and wound healing besides being required for invasive tumor growth and metastasis. Because angiogenesis sets an important point in the control of tumor progression, its inhibition is considered a valuable therapeutic approach for tumor treatment. Chronic liver disease including hepatitis C virus (HCV) infection is one of the main cause for the development of hepatic angiogenesis and thereby plays a critical role in the modulation of hepatic angiogenesis that finally leads to hepatocellular carcinoma progression and
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In recent years, several studies focused on the investigation of cellular signaling mechanisms underlying HCC development, progression and invasion. In addition to the genetic alterations, chronic liver diseases including HCV infection clearly has a major role in the development and progression of HCC. Because chronic HCV infection is implicated in the modulation of abnormalities in several critical molecular signaling pathways, the attention of clinicians and researchers has focused on the mechanistic role of HCV infection in the regulation of HCC-associated signaling pathways. These pathways include both extra and intracellular-mediated mechanisms, which among them are the MAPK, PI3K/mTOR, WNT/β-catenin and IGF, and growth factor associated angiogenic signaling. Although a direct link between HCV infection and angiogenesis has been suggested in several studies it is not clear, which factors actually drive the angiogenesis during the course of HCV infection. Further analysis is needed to address, in detail, the molecular mechanisms of HCV-induced hepatic angiogenesis. The investigation of these mechanisms may help improve current therapies and in the design of an efficient alternative approach for HCC treatment. Thus, targeting signaling pathways that are directly involved in the regulation of hepatic angiogenesis may be a powerful strategy for HCC

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