The Expanding Role of p38 Mitogen-Activated Protein Kinase in Programmed Host Cell Death

Jessica Gräb, J. Rybniker
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引用次数: 28

Abstract

The p38 mitogen-activated protein kinase (MAPK) is involved in a multitude of essential cellular processes. The kinase is activated in response to environmental stresses, including bacterial infections and inflammation, to regulate the immune response of the host. However, recent studies have demonstrated that pathogens can manipulate p38 MAPK signaling for their own benefit to either prevent or induce host cell apoptosis. In addition, there is evidence demonstrating that p38 MAPK is a potent trigger of pathogen-induced necrosis driven by mitochondrial membrane disruption. Given the large number of p38 MAPK inhibitors that have been tested in clinical trials, these findings provide an opportunity to repurpose these drugs for improved control of infectious diseases.
p38丝裂原活化蛋白激酶在程序性宿主细胞死亡中的扩展作用
p38丝裂原活化蛋白激酶(MAPK)参与了许多重要的细胞过程。该激酶在环境压力下被激活,包括细菌感染和炎症,以调节宿主的免疫反应。然而,最近的研究表明,病原体可以为自己的利益操纵p38 MAPK信号,以防止或诱导宿主细胞凋亡。此外,有证据表明p38 MAPK是由线粒体膜破坏驱动的病原体诱导的坏死的有效触发因素。鉴于大量的p38 MAPK抑制剂已经在临床试验中进行了测试,这些发现为重新利用这些药物来改善传染病的控制提供了机会。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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