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脓毒症期间细胞机制的新见解。

New insights into cellular mechanisms during sepsis.

作者信息

Hoesel Laszlo M, Gao Hongwei, Ward Peter A

机构信息

Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

出版信息

Immunol Res. 2006;34(2):133-41. doi: 10.1385/IR:34:2:133.

Abstract

Despite intensive ongoing research efforts, the mortality of patients with sepsis remains unacceptably high. Clinical trials emerging from promising results in animal models have mostly failed to deliver sufficient treatment strategies so far. Many studies investigating the underlying mechanisms of sepsis have focused on deterioration of the humoral and cellular components of the immune system. However, in addition to septic shock, the main cause of death in septic patients is multiorgan failure. So far, not much is known about the effects of a dysregulated immune system as seen in sepsis on parenchymal cells of end organs. Studies on the interaction of the complement system and kidney as well as liver cells resulted in interesting yet still inconclusive data. In this review, we provide new insights into mechanisms during sepsis based on recent findings.

摘要

尽管目前正在进行大量研究,但脓毒症患者的死亡率仍然高得令人无法接受。迄今为止,在动物模型中取得了有前景结果的临床试验大多未能提供足够的治疗策略。许多研究脓毒症潜在机制的工作都集中在免疫系统体液和细胞成分的恶化上。然而,除了感染性休克外,脓毒症患者的主要死因是多器官功能衰竭。到目前为止,对于脓毒症中出现的免疫系统失调对终末器官实质细胞的影响知之甚少。关于补体系统与肾脏以及肝细胞相互作用的研究得出了有趣但仍无定论的数据。在这篇综述中,我们基于最近的研究结果对脓毒症期间的机制提供了新的见解。

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