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首页> 外文期刊>Journal of endotoxin research >The role and regulation of apoptosis in sepsis.
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The role and regulation of apoptosis in sepsis.

机译:凋亡在脓毒症中的作用和调节。

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Today, sepsis continues to be a growing problem in the critically ill patient population. A number of laboratories have been interested in understanding how changes in immune cell apoptosis during sepsis appear to contribute to septic morbidity. Consistently, it has been found that immune cell apoptosis is altered in a variety of tissue sites and cell populations both in experimental animals and humans. While divergent mediators, such as steroids and TNF, contribute to some of these apoptotic changes, their effects are tissue and cell population selective. Inhibition of FasL-Fas signaling (by either FasL gene deficiency, in vivo gene silencing [siRNA] or with FasL binding protein) protects septic mice from the onset of marked apoptosis and the morbidity/mortality seen in sepsis. Further, this extrinsic apoptosis response appears to utilize aspects of the Bid-induced mitochondrial pathway. This is in keeping with the findings that pan-specific caspase inhibition or the overexpression of Bcl-2 also protect these animals from the sequellae of sepsis.
机译:如今,脓毒症仍然是重症患者群体中日益严重的问题。许多实验室对了解败血症期间免疫细胞凋亡的变化如何导致败血症发病率感兴趣。一致地,已经发现在实验动物和人类中,各种组织部位和细胞群中的免疫细胞凋亡都发生了改变。虽然类固醇和TNF等不同的介体会促成这些凋亡的改变,但它们的作用是对组织和细胞群的选择性。 FasL-Fas信号的抑制(通过FasL基因缺陷,体内基因沉默[siRNA]或FasL结合蛋白)可保护败血性小鼠免受明显的细胞凋亡以及败血症中所见的发病率/死亡率的影响。此外,这种外部细胞凋亡反应似乎利用了Bid诱导的线粒体途径的各个方面。这与泛特异性半胱天冬酶抑制或Bcl-2的过表达也保护这些动物免受败血症后遗症的发现相符。

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