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嘌呤能受体在多发性硬化发病机制中的作用。

Purinergic receptors in multiple sclerosis pathogenesis.

机构信息

Department of Neurosciences, University of the Basque Country, Achucarro Basque Center for Neuroscience, Instituto de Salud Carlos III, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), 48940, Leioa, Spain.

Department of Neurosciences, University of the Basque Country, Achucarro Basque Center for Neuroscience, Instituto de Salud Carlos III, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), 48940, Leioa, Spain.

出版信息

Brain Res Bull. 2019 Sep;151:38-45. doi: 10.1016/j.brainresbull.2018.11.018. Epub 2018 Nov 27.

Abstract

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system, characterized by the presence of focal lesions in white and grey matter with peripheral immune cells infiltration. Purinergic receptors control immune cell function as well as neuronal and oligodendroglial survival, and the activation of astrocytes and microglia, the endogenous brain immune cells. In particular, ionotropic purinergic receptors P2X4 and P2X7 and metabotropic receptor P2Y12 are differently expressed along the disease and their activation or blockage modifies the course of texperimental autoimmune encephalomyelitis (EAE), the dominant animal model of MS. In this review, we will summarize emerging evidence of the role of these three receptor types as potential MS biomarkers and therapeutic targets.

摘要

多发性硬化症(MS)是一种中枢神经系统的慢性炎症性脱髓鞘疾病,其特征是在白质和灰质中有局灶性病变,伴有外周免疫细胞浸润。嘌呤能受体控制免疫细胞功能以及神经元和少突胶质细胞的存活,并激活星形胶质细胞和小胶质细胞,即内源性脑免疫细胞。特别是,离子型嘌呤能受体 P2X4 和 P2X7 以及代谢型受体 P2Y12 在疾病过程中表达不同,其激活或阻断可改变实验性自身免疫性脑脊髓炎(EAE)的病程,EAE 是 MS 的主要动物模型。在这篇综述中,我们将总结这三种受体类型作为潜在 MS 生物标志物和治疗靶点的作用的新证据。

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