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首页> 外文期刊>The journal of clinical investigation >Mitochondrial Ca2+ and ROS take center stage to orchestrate TNF-α–mediated inflammatory responses
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Mitochondrial Ca2+ and ROS take center stage to orchestrate TNF-α–mediated inflammatory responses

机译：线粒体Ca2 +和ROS处于协调TNF-α介导的炎症反应的中心阶段

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Proinflammatory stimuli induce inflammation that may progress to sepsis or chronic inflammatory disease. The cytokine TNF-α is an important endotoxin-induced inflammatory glycoprotein produced predominantly by macrophages and lymphocytes. TNF-α plays a major role in initiating signaling pathways and pathophysiological responses after engaging TNF receptors. In this issue of JCI , Rowlands et al. demonstrate that in lung microvessels, soluble TNF-α (sTNF-α) promotes the shedding of the TNF-α receptor 1 ectodomain via increased mitochondrial Ca~(2+) that leads to release of mitochondrial ROS. Shedding mediated by TNF-α–converting enzyme (TACE) results in an unattached TNF receptor, which participates in the scavenging of sTNF-α, thus limiting the propagation of the inflammatory response. These findings suggest that mitochondrial Ca~(2+), ROS, and TACE might be therapeutically targeted for treating pulmonary endothelial inflammation.
机译：促炎性刺激诱发可能发展为败血症或慢性炎性疾病的炎症。细胞因子TNF-α是一种重要的内毒素诱导的炎症糖蛋白，主要由巨噬细胞和淋巴细胞产生。 TNF-α参与TNF受体后，在启动信号通路和病理生理反应中起主要作用。在JCI的这一期中，Rowlands等人。证明在肺微血管中，可溶性TNF-α（sTNF-α）通过增加线粒体Ca〜（2+）促进线粒体ROS的释放，促进TNF-α受体1胞外域的脱落。 TNF-α转换酶（TACE）介导的脱落导致未附着的TNF受体，该受体参与sTNF-α的清除，从而限制了炎症反应的传播。这些发现表明线粒体Ca〜（2 +），ROS和TACE可能是治疗肺血管内皮炎症的治疗靶点。

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