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首页> 外文期刊>Frontiers in Medicine >Neuroimmune Mechanisms in Signaling of Pain During Acute Kidney Injury (AKI)
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Neuroimmune Mechanisms in Signaling of Pain During Acute Kidney Injury (AKI)

机译:急性肾损伤期间疼痛信号传导的神经影响机制(AKI)

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Acute kidney injury (AKI) is a significant global health concern. The primary causes of AKI include ischemia, sepsis and nephrotoxicity. The unraveled interface between nervous system and immune response with specific focus on pain pathways is generating a huge interest in reference to AKI. The nervous system though static executes functions by nerve fibers throughout the body. Neuronal peptides released by nerves effect the immune response to mediate the hemodynamic system critical to the functioning of kidney. Pain is the outcome of cellular cross talk between nervous and immune systems. The widespread release of neuropeptides, neurotransmitters and immune cells contribute to bidirectional neuroimmune cross talks for pain manifestation. Recently, we have reported pain pathway genes that may pave the way to better understand such processes during AKI. An auxiliary understanding of the functions and communications in these systems will lead to novel approaches in pain management and treatment through the pathological state, specifically during acute kidney injury.
机译:急性肾脏损伤(AKI)是一项重大的全球健康问题。 AKI的主要原因包括缺血,败血症和肾毒性。神经系统与免疫反应之间的解开界面与特异性关注疼痛途径产生巨大的兴趣。神经系统虽然静态执行整个神经纤维的功能。神经释放的神经元肽影响免疫应答,使血液动力学系统介导对肾脏功能关键。疼痛是神经和免疫系统之间细胞交叉谈话的结果。神经肽,神经递质和免疫细胞的广泛释放有助于对疼痛表现的双向神经影响交叉谈判。最近,我们报道了止痛途径基因,可以在AKI期间更好地了解此类过程。对这些系统中的功能和通信的辅助理解将导致疼痛管理和通过病理状态治疗的新方法,特别是在急性肾损伤期间。

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