内切酶在肾小管上皮细胞损伤中的作用。

N Ueda, S V Shah
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引用次数: 12

摘要

细胞死亡的研究已成为细胞生物学中一个重要而令人兴奋的研究领域。虽然细胞凋亡和坏死这两种类型的细胞死亡是公认的,但我们对细胞死亡的理解的主要进展之一是认识到传统上与细胞凋亡相关的途径可能在与坏死相关的细胞损伤形式中非常关键。肾小管上皮细胞因缺血或毒素引起的损伤通常被认为是细胞死亡的一种坏死形式。我们简要地描述了最近的证据表明凋亡机制,包括内切酶激活肾小管损伤和一些调节这一过程的介质(氧化剂,半胱天冬酶和神经酰胺)。细胞所遵循的途径取决于损伤的性质和严重程度,导致细胞死亡的凋亡或坏死模式的级联反应可能几乎同时被激活,并且可能有一些共同的途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of endonucleases in renal tubular epithelial cell injury.

The study of cell death has emerged as an important and exciting area of research in cell biology. Although two kinds of cell death, apoptosis and necrosis, are recognized, one of the major advances in our understanding of cell death has been the recognition that the pathways traditionally associated with apoptosis may be very critical in the form of cell injury associated with necrosis. Renal tubular epithelial cell injury from ischemia or toxins has generally been regarded as a result of a necrotic form of cell death. We briefly describe recent evidence indicating apoptotic mechanisms including endonuclease activation in renal tubular injury and some mediators (oxidants, caspases and ceramide) which regulate this process. The pathway that is followed by the cell is dependent on both the nature and severity of insults, and it is likely that the cascades that lead to the apoptotic or necrotic mode of cell death are activated almost simultaneously and may share some common pathways.

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