Abstract
Liver cell injury and cell death are prominent features in the pathogenesis of acute liver failure. Mitochondrial Uncoupling Protein 2 (UCP2) plays a controversial role in liver cell death through its involvement in the production of reactive oxygen species and adenosine triphosphate. The present study was designed to investigate the exact role of UCP2 in the pathogenesis of endotoxemic acute liver failure using UCP2-deficient mice challenged with D-galactosamine and Escherichia coli lipopolysaccharide. UCP2-deficient mice exhibited higher rates of hepatocellular apoptosis, however better preserved hepatic sinusoidal perfusion, milder inflammatory reaction, less necrotic injury, lower levels of transaminases and finally better survival rates. As net result, UCP2 deficiency provided protection under endotoxemic stress conditions, which underlines the significant role of the bioenergetic status in critical illness.
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