Manifestation of renin angiotensin system modulation in traumatic brain injury.
Manifestation of renin angiotensin system modulation in traumatic brain injury.
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DOI：
10.1007/s11011-021-00728-1
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发表时间：
2021-08
影响因子：
3.6
通讯作者：
Ishrat T
中科院分区：
文献类型：
--
作者：
Mirzahosseini G;Ismael S;Ahmed HA;Ishrat T
创伤性脑损伤(TBI)改变了脑功能，是世界范围内一个重要的公共卫生问题。创伤性脑损伤触发炎症介质(细胞因子)的释放，加重脑损伤，从而影响临床预后。肾素血管紧张素系统(RAS)在颅脑损伤的病理生理学中起着重要作用。RAS在包括大脑在内的许多器官中广泛表达。血管紧张素转换酶1(AT1)和血管紧张素转换酶2(AT2)受体信号对脑内RAS的调节作用影响包括脑损伤在内的许多病理生理过程。AT1R在神经元和星形胶质细胞中高表达。AT1R的上调介导了血管紧张素II(Ang II)的作用，包括促炎细胞因子的释放、细胞死亡、氧化应激和血管收缩。AT2R主要在发育过程中的胎儿大脑表达，也与认知功能有关。激活这一受体通路可减少神经炎症和氧化应激，并提高整体细胞存活率。大量研究表明，抑制AT1R和激活AT2R对脑外伤的治疗效果各不相同。在这篇综述中，我们综述了脑内RAS信号通过AT1R和AT2R在脑损伤中的作用，以及用药理学方法对其进行调控的研究。
Traumatic brain injury (TBI) alters brain function and is a crucial public health concern worldwide. TBI triggers the release of inflammatory mediators (cytokines) that aggravate cerebral damage, thereby affecting clinical prognosis. The renin angiotensin system (RAS) plays a critical role in TBI pathophysiology. RAS is widely expressed in many organs including the brain. Modulation of the RAS in the brain via angiotensin type 1 (AT1) and type 2 (AT2) receptor signaling affects many pathophysiological processes, including TBI. AT1R is highly expressed in neurons and astrocytes. The upregulation of AT1R mediates the effects of angiotensin II (ANG II) including release of proinflammatory cytokines, cell death, oxidative stress, and vasoconstriction. The AT2R, mainly expressed in the fetal brain during development, is also related to cognitive function. Activation of this receptor pathway decreases neuroinflammation and oxidative stress and improves overall cell survival. Numerous studies have illustrated the therapeutic potential of inhibiting AT1R and activating AT2R for treatment of TBI with variable outcomes. In this review, we summarize studies that describe the role of brain RAS signaling, through AT1R and AT2R in TBI, and its modulation with pharmacological approaches.
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影响因子：
5.4
作者：
Hirooka, Y;Kimura, Y;Sunagawa, K
通讯作者：
Sunagawa, K
影响因子：
7.3
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DOI：
10.18632/aging.101419
发表时间：
2018-04-17
期刊：
Aging
影响因子：
--
作者：
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通讯作者：
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影响因子：
7.4
作者：
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通讯作者：
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