创伤性脑损伤
星形胶质细胞
内皮素
神经营养因子
内皮素受体
神经炎症
医学
受体
神经营养素
内科学
神经科学
内分泌学
中枢神经系统
炎症
心理学
精神科
作者
Shotaro Michinaga,Shigeru Hishinuma,Yutaka Kōyama
出处
期刊:Cells
[Multidisciplinary Digital Publishing Institute]
日期:2023-02-24
卷期号:12 (5): 719-719
被引量:9
标识
DOI:10.3390/cells12050719
摘要
Traumatic brain injury (TBI) is an intracranial injury caused by accidents, falls, or sports. The production of endothelins (ETs) is increased in the injured brain. ET receptors are classified into distinct types, including ETA receptor (ETA-R) and ETB receptor (ETB-R). ETB-R is highly expressed in reactive astrocytes and upregulated by TBI. Activation of astrocytic ETB-R promotes conversion to reactive astrocytes and the production of astrocyte-derived bioactive factors, including vascular permeability regulators and cytokines, which cause blood–brain barrier (BBB) disruption, brain edema, and neuroinflammation in the acute phase of TBI. ETB-R antagonists alleviate BBB disruption and brain edema in animal models of TBI. The activation of astrocytic ETB receptors also enhances the production of various neurotrophic factors. These astrocyte-derived neurotrophic factors promote the repair of the damaged nervous system in the recovery phase of patients with TBI. Thus, astrocytic ETB-R is expected to be a promising drug target for TBI in both the acute and recovery phases. This article reviews recent observations on the role of astrocytic ETB receptors in TBI.
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