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酸性鞘磷脂酶/神经酰胺系统作为缺血性中风治疗的靶点

The Acid Sphingomyelinase/ Ceramide System as Target for Ischemic Stroke Therapies.

作者信息

Mohamud Yusuf Ayan, Hagemann Nina, Hermann Dirk M

机构信息

Department of Neurology, University Hospital Essen, Essen, Germany.

Department of Neurology, University Hospital Essen, Essen, Germany,

出版信息

Neurosignals. 2019;27(S1):32-43. doi: 10.33594/000000184.

Abstract

In this review, we summarize implications of the acid sphingomyelinase/ ceramide system in ischemic stroke. Acid sphingomyelinase catalyzes the formation of the bioactive sphingolipid ceramide which coalesces into membrane platforms and has a pivotal role in inflammation, cell signaling and death. Cerebral ischemia increases acid sphingomyelinase activity and elevates brain ceramide levels, which has been associated with the exacerbation of ischemic injury and deterioration of stroke outcome. In view of the fact that lowering acid sphingomyelinase activity and ceramide level was shown to protect against ischemic injury and ameliorate neurological deficits, the acid sphingomyelinase/ ceramide system might represent a promising target for stroke therapies.

摘要

在本综述中,我们总结了酸性鞘磷脂酶/神经酰胺系统在缺血性卒中中的意义。酸性鞘磷脂酶催化生物活性鞘脂神经酰胺的形成,神经酰胺聚集成膜平台,并在炎症、细胞信号传导和死亡中起关键作用。脑缺血会增加酸性鞘磷脂酶活性并升高脑内神经酰胺水平,这与缺血性损伤的加重和卒中预后的恶化有关。鉴于降低酸性鞘磷脂酶活性和神经酰胺水平可预防缺血性损伤并改善神经功能缺损,酸性鞘磷脂酶/神经酰胺系统可能是卒中治疗的一个有前景的靶点。

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