Apoptosis in nonalcoholic fatty liver disease: diagnostic and therapeutic implications.

Apoptosis in nonalcoholic fatty liver disease: diagnostic and therapeutic implications.
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DOI:
10.1586/egh.11.6
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发表时间:
2011-04
影响因子:
3.9
通讯作者:
Feldstein AE
Feldstein AE
中科院分区:
医学3区
文献类型:
--
作者:
Alkhouri N;Carter-Kent C;Feldstein AE

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肝脏和周围组织中细胞死亡的病理性增加已成为非酒精性脂肪性肝病(NAFLD)发生发展的重要机制。在NAFLD患者和实验性脂肪性肝炎模型中,肝细胞因凋亡而死亡的增加是典型的,而内脏脂肪组织中脂肪细胞死亡的增加可能是触发胰岛素抵抗和肝脏脂肪变性的重要机制。细胞凋亡的两条基本途径,即外源性途径(死亡受体介导的)和内在途径(细胞器启动),都参与其中。本文综述了NAFLD发病机制中细胞死亡的不同分子和生化途径的相关知识。特别是,它将强调在这一知识的基础上开发新的诊断和治疗战略的努力。
Pathological increases in cell death in the liver as well as in peripheral tissues has emerged as an important mechanism involved in the development and progression of nonalcoholic fatty liver disease (NAFLD). An increase in hepatocyte cell death by apoptosis is typically present in patients with NAFLD and in experimental models of steatohepatitis, while an increase in adipocyte cell death in visceral adipose tissue may be an important mechanism triggering insulin resistance and hepatic steatosis. The two fundamental pathways of apoptosis, the extrinsic (death receptor-mediated) and intrinsic (organelle-initiated) pathways, are both involved. This article summarizes the current knowledge related to the distinct molecular and biochemical pathways of cell death involved in NAFLD pathogenesis. In particular, it will highlight the efforts for the development of both novel diagnostic and therapeutic strategies based on this knowledge.
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