Mechanisms and clinical implications of hepatocyte lipoapoptosis.
Mechanisms and clinical implications of hepatocyte lipoapoptosis.
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DOI：
10.2217/clp.09.85
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发表时间：
2010-02-01
影响因子：
--
通讯作者：
Gores GJ
中科院分区：
文献类型：
--
作者：
Cazanave SC;Gores GJ
非酒精性脂肪性肝病（NAFLD）的特征在于胰岛素抵抗、血清游离脂肪酸（FFA）水平升高和肝脏脂肪浸润。肝细胞中甘油三酯的蓄积是由于肝脏对循环FFA的摄取和酯化所致。与目前的理论相反，肝脂肪变性似乎是一个解毒过程，因为FFA对肝细胞具有直接细胞毒性，抑制甘油三酯形成会增强FFA的毒性。肝细胞凋亡是NAFLD的一个关键特征，与疾病严重程度相关。由于FFA诱导的毒性，或脂肪细胞凋亡，代表了NAFLD的发病机制，本文将强调细胞途径有助于肝细胞脂肪细胞凋亡。迄今为止，对于NAFLD患者还没有被证明有效的治疗方法，对脂凋亡分子介质的了解应该有助于促进这种疾病的有效治疗策略。
Nonalcoholic fatty liver disease (NAFLD) is characterized by insulin resistance, elevated serum levels of free fatty acids (FFAs) and fatty infiltration of the liver. Accumulation of triglycerides in the hepatocyte results from the uptake and esterification of circulating FFAs by the liver. Contrary to current theory, hepatic steatosis appears to be a detoxification process, as FFAs are directly cytotoxic for the hepatocyte and inhibition of triglyceride formation enhances FFAs toxicity. Hepatocyte apoptosis is a key feature of NAFLD and correlates with disease severity. Since FFA-induced toxicity, or lipoapoptosis, represents a mechanism for the pathogenesis of NAFLD, this article will highlight the cellular pathways contributing to hepatocyte lipoapoptosis. To date, there is no proven effective therapy for patients with NAFLD and insights into the molecular mediators of lipoapoptosis should help promote effective therapeutic strategies for this disease.
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