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脓毒症中磷酸肌醇-3 激酶生存信号机制。

The phosphoinositide-3 kinase survival signaling mechanism in sepsis.

机构信息

Clarian Cardiovascular Surgery, Methodist Hospital, Indianapolis, Indiana, USA.

出版信息

Shock. 2010 Nov;34(5):442-9. doi: 10.1097/SHK.0b013e3181e14ea9.

DOI:10.1097/SHK.0b013e3181e14ea9
PMID:20386497
Abstract

Phosphoinositide-3 kinases (PI3Ks) are critical regulatory proteins in the immunologic defense system against sepsis. The PI3K mechanism helps modulate cellular survival, innate and adaptive immunities, inflammation, nuclear factor-κB transcription, and may, in turn, play a protective role in sepsis. Animal studies confirm its role in the prevention of organ dysfunction and improvement of survival outcomes. Further advances in the understanding of this key immunomodulatory pathway may provide valuable insights into the manipulation of cellular function for therapeutic treatment of sepsis and other inflammatory diseases.

摘要

磷酸肌醇 3 激酶(PI3Ks)是对抗败血症的免疫防御系统中的关键调节蛋白。PI3K 机制有助于调节细胞存活、先天和适应性免疫、炎症、核因子-κB 转录,并且反过来可能在败血症中发挥保护作用。动物研究证实了其在预防器官功能障碍和改善生存结果中的作用。对这一关键免疫调节途径的进一步深入了解,可能为操纵细胞功能提供有价值的见解,从而治疗败血症和其他炎症性疾病。

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