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Potential mechanisms of hepatitis B virus induced liver injury 被引量:13
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作者 Mohd Suhail Hany abdel-Hafiz +5 位作者 ashraf ali Kaneez Fatima ghazi a damanhouri Esam azhar adeel Ga Chaudhary Ishtiaq Qadri 《World Journal of Gastroenterology》 SCIE CAS 2014年第35期12462-12472,共11页
Chronic active hepatitis(CAH) is acknowledged as an imperative risk factor for the development of liver injury and hepatocellular carcinoma.The histological end points of CAH are chronic inflammation,fibrosis and cirr... Chronic active hepatitis(CAH) is acknowledged as an imperative risk factor for the development of liver injury and hepatocellular carcinoma.The histological end points of CAH are chronic inflammation,fibrosis and cirrhosis which are coupled with increased DNA synthesis in cirrhotic vs healthy normal livers.The potential mechanism involved in CAH includes a combination of processes leading to liver cell necrosis,inflammation and cytokine production and liver scaring(fibrosis).The severity of liver damage is regulated by Hepatitis B virus genotypes and viral components.The viral and cellular factors that contribute to liver injury are discussed in this article.Liver injury caused by the viral infection affects many cellular processes such as cell signaling,apoptosis,transcription,DNA repair which in turn induce radical effects on cell survival,growth,transformation and maintenance.The consequence of such perturbations is resulted in the alteration of bile secretion,gluconeogenesis,glycolysis,detoxification and metabolism of carbohydrates,proteins,fat and balance of nutrients.The identification and elucidation of the molecular pathways perturbed by the viral proteins are important in order to design effective strategy to minimize and/or restore the hepatocytes injury. 展开更多
关键词 Hepatitis B virus Hepatitis B virus genotype Hepatocellular carcinoma Woodchuck hepatitis virus Ground squirrel hepatitis virus Peripheral blood mononuclear cells Interferon regulatory factor 7 Interleukin-1 receptor-associated kinase 4 TNF receptor-associated factor 3
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