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氧化型肝损伤中的蛋白激酶C信号传导

PKC signaling in oxidative hepatic damage.

作者信息

Nitti Mariapaola, Pronzato Maria A, Marinari Umberto M, Domenicotti Cinzia

机构信息

Department of Experimental Medicine, General Pathology Section, L.B. Alberti 2, 16132 Genoa, Italy.

出版信息

Mol Aspects Med. 2008 Feb-Apr;29(1-2):36-42. doi: 10.1016/j.mam.2007.09.001. Epub 2007 Oct 7.

DOI:10.1016/j.mam.2007.09.001
PMID:18035409
Abstract

Protein kinase C (PKC) is a family of isoenzymes differently involved in cell response to injury and many studies describe their role as "stress sensors". Oxidative stress is strictly involved in the pathogenesis of chronic liver diseases including alcohol- or drug-induced hepatotoxicity, iron overload, hepatitis and hepatocarcinoma development, but molecular mechanisms are not really defined. A crucial role of PKC as a redox sensitive signaling molecule has been widely accepted.

摘要

蛋白激酶C（PKC）是一组同工酶，它们在细胞对损伤的反应中发挥着不同的作用，许多研究将它们的作用描述为“应激传感器”。氧化应激与包括酒精或药物诱导的肝毒性、铁过载、肝炎和肝癌发生在内的慢性肝病发病机制密切相关，但分子机制尚未明确界定。PKC作为一种氧化还原敏感信号分子的关键作用已被广泛认可。

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