急性呼吸窘迫综合征
创伤性脑损伤
医学
间隙
弥漫性肺泡损伤
薄壁组织
血脑屏障
胞外囊泡
肺水肿
肺
急性呼吸窘迫
病理
免疫学
内科学
微泡
中枢神经系统
生物
小RNA
精神科
基因
生物化学
作者
Qiujie Wang,Fanjian Li,Ziqi Zhao,Jianning Zhang
出处
期刊:American Journal of Physiology-lung Cellular and Molecular Physiology
[American Physiological Society]
日期:2021-11-01
卷期号:321 (5): L885-L891
被引量:14
标识
DOI:10.1152/ajplung.00023.2021
摘要
Acute lung injury (ALI), a common complication after traumatic brain injury (TBI), can evolve into acute respiratory distress syndrome (ARDS) and has a mortality rate of 30%-40%. Secondary ALI after TBI exhibits the following typical pathological features: infiltration of neutrophils into the alveolar and interstitial space, alveolar septal thickening, alveolar edema, and hemorrhage. Extracellular vesicles (EVs) were recently identified as key mediators in TBI-induced ALI. Due to their small size and lipid bilayer, they can pass through the disrupted blood-brain barrier (BBB) into the peripheral circulation and deliver their contents, such as genetic material and proteins, to target cells through processes such as fusion, receptor-mediated interactions, and uptake. Acting as messengers, EVs contribute to mediating brain-lung cross talk after TBI. In this review, we aim to summarize the mechanism of EVs in TBI-induced ALI, which may provide new ideas for clinical treatment.
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