Function of aquaporins in sepsis: a systematic review.

Function of aquaporins in sepsis: a systematic review.
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DOI:
10.1186/s13578-018-0211-9
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发表时间:
2018
期刊:
影响因子:
7.5
通讯作者:
Adamzik M
Adamzik M
中科院分区:
生物学2区
文献类型:
--
作者:
Rump K;Adamzik M

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脓毒症是全世界重症监护病房的常见死亡原因。由于这种免疫综合征的高度复杂性,迫切需要开发新的治疗策略。有前途的药物靶点或生物标志物可以描述水通道蛋白(AQP),因为它们调节脓毒症的关键机制。在此,我们报告的基础上,目前的文献,几个AQPs参与不同的生理过程中的脓毒症。在免疫系统中,主要是AQP 3、5和9似乎是重要的,因为它们调节不同免疫细胞的迁移。几项研究表明,AQP3是T细胞功能和巨噬细胞迁移所必需的,AQP5和AQP9调节中性粒细胞迁移并影响脓毒症存活。此外,AQP 1和5在免疫系统中的功能在脓毒症诱导的肺损伤中起作用,并且它们在炎症刺激损害肺损伤后下调。相比之下,AQP4表达在脑炎症过程中上调,并加重脓毒症中的脑水肿。在肾脏中,AQP2表达在脓毒症期间下调,并且可导致肾衰竭。一些研究还表明AQP 1在心脏功能中的作用。总之,水通道蛋白参与了脓毒症的多种生理功能障碍,其表达受到不同程度的调节。对水通道蛋白调控机制的进一步研究可能会发现潜在的治疗靶点。
Sepsis is a common cause of death in intensive care units worldwide. Due to the high complexity of this immunological syndrome development of novel therapeutic strategies is urgent. Promising drug targets or biomarkers may depict aquaporins (AQPs) as they regulate crucial key mechanisms of sepsis. Here we report on base of the current literature that several AQPs are involved in different physiological processes of sepsis. In immune system mainly AQPs 3, 5 and 9 seem to be important, as they regulate the migration of different immune cells. Several studies showed that AQP3 is essential for T cell function and macrophage migration and that AQP5 and AQP9 regulate neutrophil cell migration and impact sepsis survival. Additionally, to the function in immune system AQPs 1 and 5 play a role in sepsis induced lung injury and their downregulation after inflammatory stimuli impair lung injury. By contrast, AQP4 expression is up-regulated during brain inflammation and aggravates brain edema in sepsis. In kidney AQP2 expression is downregulated during sepsis and can cause renal failure. Some studies also suggest a role of AQP1 in cardiac function. In conclusion, AQPs are involved in many physiological dysfunctions in sepsis and their expressions are differently regulated. Additional research on the regulatory mechanisms of aquaporins may identify potential therapeutic targets.
脓毒症心肌病的线粒体机制。
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