http://www.cnr.it/ontology/cnr/individuo/prodotto/ID62789
Molecular basis and mechanisms of progression of non-alcoholic steatohepatitis (Articolo in rivista)
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- Label
- Molecular basis and mechanisms of progression of non-alcoholic steatohepatitis (Articolo in rivista) (literal)
- Anno
- 2008-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.molmed.2007.12.003 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Marra F.; Gastaldelli A.; Svegliati Baroni G.; Tell G.; Tiribelli C. (literal)
- Pagina inizio
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
- http://www.ncbi.nlm.nih.gov/pubmed/18218340 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
- In: Trends Moecular Medicine, vol. 14 (2) pp. 72 - 81. Elsevier Ltd, 2008. (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
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- ISI Web of Science (WOS) (literal)
- PubMe (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- 1. Univ Trieste, Ctr Studi Fegato, I-34127 Trieste, Italy
2. Univ Trieste, Dept BBCM, I-34127 Trieste, Italy
3. Univ Florence, Dipartimento Med Interna, I-50134 Florence, Italy
4. Univ Florence, Ctr Ric Transferimento & Alta Formaz Deno THE, I-50134 Florence, Italy
5. CNR, Ist Fisiol Clin, I-56124 Pisa, Italy
6. Univ Udine, Dipartimento Sci & Tecnol Biomed, I-33100 Udine, Italy
7. Univ Marche, Dipartimento Gastroenterol, I-60020 Ancona, Italy (literal)
- Titolo
- Molecular basis and mechanisms of progression of non-alcoholic steatohepatitis (literal)
- Abstract
- Non-alcoholic steatohepatitis (NASH), a cause of cirrhosis and hepatocellular carcinoma, is characterized by fatty infiltration of the liver, inflammation, hepatocellular damage and fibrosis. Progress has been made in understanding the molecular and cellular mechanisms implicated in the pathogenesis of this condition, therefore, we here review recent developments regarding the basic mechanisms of NASH development. Accumulation of triglycerides in the hepatocytes is the result of increased inflow of free fatty acids and de novo lipogenesis. Steatosis leads to lipotoxicity, which causes apoptosis, necrosis, generation of oxidative stress and inflammation. The resulting chronic injury activates a fibrogenic response that leads eventually to end-stage liver disease. A better understanding of these mechanisms is crucial for the design of novel diagnostic and therapeutic strategies. (literal)
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