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 Printable version |
Autophagy in liver diseases |
Hépato-Gastro. Volume 18, Number 4, 398-403, Juillet-Août 2011, Mini-revue
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 Résumé
Texte intégral
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Author(s) : Pierre-Emmanuel Rautou, Dominique Valla, Richard Moreau |
Summary : Autophagy, or cellular self-digestion, is a cellular pathway crucial for development, differentiation, survival, and homeostasis. Its implication in human diseases has been highlighted during the last decade. Recent data show that autophagy is involved in major fields of hepatology. In liver ischemia reperfusion injury, autophagy has mainly a prosurvival activity allowing the cell for coping with nutrient starvation and anoxia. During hepatitis B or C infection, autophagy is also increased but subverted by viruses for their own benefit. In hepatocellular carcinoma, autophagy has an antitumor role and therapeutic strategies increasing autophagy, as rapamycin, have a beneficial effect. Moreover, in hepatocellular carcinoma, beclin-1 level, an autophagy protein, has a prognostic significance. In α-1 antitrypsin deficiency, the aggregation-prone ATZ protein accumulates in the endoplasmic reticulum. This activates the autophagic response, which contributes to degradation of mutant ATZ. Increasing autophagy in patients with α-1 antitrypsin deficiency could be a therapeutic option. Following alcohol consumption, autophagy is diminished in liver cells likely due to a decrease in adenosine monophosphate-activated protein kinase (AMPk) and to an alteration in vesicle transport in hepatocytes. This decrease in autophagy contributes to the formation of Mallory-Denk bodies and to liver cell death. Autophagy is thus a crucial pathway in many liver diseases and could be a new therapeutic target. |
Keywords : autophagic vacuole, autophagosome, hepatitis, hepatocellular carcinoma, LC3, starvation |
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