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Modulation of CD95 (APO-1/Fas)-induced hepatocyte death by NO

机译:CD95(APO-1 / Fas)的调节 - 诱导肝细胞死亡

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During recent years, a significant body of evidence has accumulated supporting the role of apoptosis and, particularly, of the CD95 death receptor-ligand system in liver disease. Many non-lymphoid tissues, such as the liver, constitutively express CD95 and are thus sensitive to activation by CD95L. The cell-surface receptor CD95 (APO-1/Fas) is a major trigger of apoptosis and cells rapidly undergo apoptotic cell death upon CD95 stimulation via GD95L or agonistic antibodies. The importance of the CD95 system in liver pathophysiology and homeostasis is well documented. We have described in different forms of acute and chronic liver failure, including viral infections, alcoholic liver damage, Wilson's disease and others, that deregulation of the CD95 receptor and/or lig-and is causally involved in disease progression. Lymphocytes as well as liver cells themselves have been identified as pathogenetic relevant sources of CD95L in liver disease. Further support for an important role of CD95 in the liver comes from studies using animal models in which it has been demonstrated that interruption of CD95/CD95L interaction prevents liver damage.
机译:近年来,一系列重要的证据积累了肝脏疾病中CD95死亡受体 - 配体系统的作用。许多非淋巴组织,例如肝脏,组成思考CD95,因此对CD95L的活化敏感。细胞表面受体CD95(apo-1 / Fas)是细胞凋亡和细胞的主要触发,并且通过GD95L或激动抗体在CD95刺激时迅速进行凋亡细胞死亡。 CD95系统在肝脏病理生理学和稳态中的重要性有很好的记录。我们已经以不同形式的急性和慢性肝衰竭描述,包括病毒感染,酒精性肝脏损伤,威尔逊疾病和其他疾病,对CD95受体和/或LIG的放松管制症,并导致疾病进展。淋巴细胞以及肝细胞本身已被鉴定为肝病中CD95L的致病相关来源。进一步支持CD95在肝脏中的重要作用来自使用动物模型的研究,其中已经证明CD95 / CD95L相互作用的中断可防止肝损伤。

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