The role of hepatitis C virus (HCV) infection in the development of vascular disease is controversial. Insulin resistance (IR) is a recognized risk factor for cardiovascular disease (CVD) and is associated with chronic hepatitis C (CHC). Thus, IR may promote atherosclerosis and vascular disease in CHC patients. HCV-associated IR may also cause hepatic steatosis and resistance to antiviral treatment. In addition, HCV may contribute a direct, proatherogenetic action on the vascular wall. This review considers the impact of IR on interferon-α based therapy of HCV infection and the role of insulin-sensitizing agents on the response to antiviral treatment and prevention of IR complications, including CVD.
Keywords: Hepatitis C, insulin resistance, interferon-α, vascular disease, oxidative stress, Interferon (INF), interferon-receptor, Jak/STAT, ISGF3, HOMA-IR, SOCS3, protein phosphatase 2A, PIAS1, protein arginine methyl-transferase (PRMT1), B kinase-beta (IKK), Etanercept, TNF-protein, T1DM, T2DM, HEPATIC STEATOSIS (HS), metabolic steatosis, non alcoholic fatty liver disease, Thiazolidinediones, pioglitazone, rosiglitazone, peroxisome proliferator activated receptors, PPAR- mRNA, STATIN THERAPY AND CHC
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