期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 321, 期 5, 页码 L885-L891出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00023.2021
关键词
acute lung injury; coagulation; extracellular vesicle; inflammation; traumatic brain injury
资金
- National Natural Science Foundation of China [82022020, 81971176, 81930031, 81720108015]
- Tianjin Research Innovation Project for Postgraduate Students, Key Laboratory of Central Nerve Injury Repair and Regeneration of Ministry of Education [2019YJSS183]
Acute lung injury (ALI) following traumatic brain injury (TBI) can progress to acute respiratory distress syndrome (ARDS) with a high mortality rate. Extracellular vesicles (EVs) have been identified as key mediators in TBI-induced ALI, potentially offering new insights for clinical treatment.
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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