Going up in flames: necrotic cell injury and inflammatory diseases.
Going up in flames: necrotic cell injury and inflammatory diseases.
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DOI：
10.1007/s00018-010-0413-8
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发表时间：
2010-10
影响因子：
8
通讯作者：
Chan, Francis Ka-Ming
中科院分区：
文献类型：
--
作者：
Challa, Sreerupa;Chan, Francis Ka-Ming
最近的证据表明，细胞死亡可以通过多种机制诱导。值得注意的是，相同的死亡信号通常可以诱导细胞的凋亡性和非凋亡性死亡。例如，抑制半胱氨酸天冬氨酸酶通常会将一种促凋亡的刺激转化为一种导致坏死的刺激。由于坏死性细胞损伤需要一种不同于控制细胞凋亡的专用分子回路，因此“程序性坏死”或“坏死性下垂”等术语被用来区分由非特异性创伤(如热休克)或由细胞凋亡引起的继发性坏死引起的刺激依赖性坏死。在几个实验模型中，程序性坏死/坏死性下垂已被证明是病原体或损伤诱导的炎症的关键控制点。本文就程序性坏死/坏死性下垂的调控机制及其在病原体感染、药物性细胞损伤和创伤后组织损伤中的生物学意义作一综述。
Recent evidence indicates that cell death can be induced through multiple mechanisms. Strikingly, the same death signal can often induce apoptotic as well as non-apoptotic cell death. For instance, inhibition of caspases often converts an apoptotic stimulus to one that causes necrosis. Because a dedicated molecular circuitry distinct from that controlling apoptosis is required for necrotic cell injury, terms such as “programmed necrosis” or “necroptosis” have been used to distinguish stimulus-dependent necrosis from those induced by non-specific traumas (e.g. heat shock) or secondary necrosis induced as a consequence of apoptosis. In several experimental models, programmed necrosis/necroptosis has been shown to be a crucial control point for pathogen- or injury-induced inflammation. In this review, we will discuss the molecular mechanisms that regulate programmed necrosis/necroptosis and its biological significance in pathogen infections, drug-induced cell injury and trauma-induced tissue damage.
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影响因子：
5.4
作者：
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通讯作者：
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影响因子：
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作者：
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影响因子：
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作者：
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