Mitochondrial injury, oxidative stress, and antioxidant gene expression are induced by hepatitis C virus core protein.

By M. Okuda, Kui Li, M. Beard, Lori Showalter, F. Scholle, S. Lemon, S. Weinman. Gastroenterology, 2002

983 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Insulin resistance in chronic hepatitis C: association with genotypes 1 and 4, serum HCV RNA level, and liver fibrosis. (2008, background): “ssociated with steatosis and not IR in multivariate analsis20 –22; (2) IR was not tested as an independent predicor of fibrosis27–29; and (3) serum C-peptide was not vailable; therefore, insulin secretion could not have been valuated, and hyperinsulinemia in relation to reduced epatic insulin extrac”
Immunobiology and pathogenesis of viral hepatitis. (2006, background): “Finally, it has also been suggested that the steatotic process may be facilitated by HCV core protein accumulation within mitochondria; this accumulation may subsequently induce oxidative stress and perturb lipid metabolism (30, 33).”
iArc monogrAphs on the evAluAtion oF cArcinogenic risks to humAns (2012, background): “Apart from the importance of hepatocyte necrosis and regeneration in generating oxidative damage, the HCV core and NS5a proteins have been reported to directly generate reactive oxygen species (Gong et al., 2001; Okuda et al., 2002).”
Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “Moreover, hepatocyte expression of HCV core protein is associated with decreased intracellular and mitochondrial glutathione levels, an important antioxidant [178,179].”