International journal of nanomedicine · 2025
Apoptotic Vesicles Attenuate Acute Lung Injury via CD73-Mediated Inhibition of Platelet Activation and NETosis.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Tan Lingping, Zhang Chi, Kou Xiaoxing, Zhao Lu, Wu Di, Li Jinyu, Yu Chuanying, Xu Tansi, Gao Li, Mao Xueli, Zhao Chuanjiang
Аннотация
INTRODUCTION: Acute respiratory distress syndrome (ARDS) is a life-threatening type of acute lung injury (ALI) characterized by elevated mortality rates and long-term effects. To date, no pharmacological treatment has proven effective for ARDS. Mesenchymal stem cell-derived apoptotic vesicles (apoVs) were recently found to have excellent therapeutic potential for inflammatory diseases. In this study, our aim was to investigate the therapeutic effects and underlying mechanisms of apoVs in ALI.
METHODS: ALI was induced in mice through intratracheal instillation of lipopolysaccharide (LPS). ApoVs were then administered two hours post-induction, and their impacts on platelet activation, neutrophil infiltration, and NETosis were assessed. Additionally, the role of CD73 in mediating these effects was thoroughly investigated.
RESULTS: ApoVs inhibit platelet activation, thereby impeding the infiltration of neutrophils into the lung and the initiation of NETosis, ultimately alleviating ALI. Remarkably, apoVs were enriched with CD73, which was critical for apoV-mediated repression of platelet activation and neutrophil NETosis, as well as the therapeutic effects observed in lung injury.
CONCLUSION: This study reveals that apoVs inhibit platelet activity and neutrophil NETosis via CD73, offering an innovative and effective cell-free therapeutic strategy for ALI/ARDS.
METHODS: ALI was induced in mice through intratracheal instillation of lipopolysaccharide (LPS). ApoVs were then administered two hours post-induction, and their impacts on platelet activation, neutrophil infiltration, and NETosis were assessed. Additionally, the role of CD73 in mediating these effects was thoroughly investigated.
RESULTS: ApoVs inhibit platelet activation, thereby impeding the infiltration of neutrophils into the lung and the initiation of NETosis, ultimately alleviating ALI. Remarkably, apoVs were enriched with CD73, which was critical for apoV-mediated repression of platelet activation and neutrophil NETosis, as well as the therapeutic effects observed in lung injury.
CONCLUSION: This study reveals that apoVs inhibit platelet activity and neutrophil NETosis via CD73, offering an innovative and effective cell-free therapeutic strategy for ALI/ARDS.