Liu Gang, Dong Bin-Bin, Devanarayana Shalika, Chen Rong-Chang, Liu Qi
Department of Emergency Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Translational Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Front Immunol. 2024 Nov 27;15:1479230. doi: 10.3389/fimmu.2024.1479230. eCollection 2024.
The pathogenetic mechanisms of ventilator-induced lung injury (VILI) still need to be elucidated. The mechanical forces during mechanical ventilation are continually sensed and transmitted by mechanosensitive ion channels (MSICs) in pulmonary endothelial, epithelial, and immune cells. In recent years, MSICs have been shown to be involved in VILI.
A systematic search across PubMed, the Cochrane Library, Web of Science, and ScienceDirect was performed from inception to March 2024, and the review was conducted in accordance with PRISMA guidelines. The potential eligible studies were evaluated by two authors independently. Study characteristics, quality assessment, and potential mechanisms were analyzed.
We included 23 eligible studies, most of which were performed with murine animals . At the level, 52% and 48% of the experiments were conducted with human or animal cells, respectively. No clinical studies were found. The most reported MSICs include Piezo channels, transient receptor potential channels, potassium channels, and stretch-activated sodium channels. Piezo1 has been the most concerned channel in the recent five years. This study found that signal pathways, such as RhoA/ROCK1, could be enhanced by cyclic stretch-activated MSICs, which contribute to VILI through dysregulated inflammation and immune responses mediated by ion transport. The review indicates the emerging role of MSICs in the pathogenesis of VILI, especially as a signal-transmitting link between mechanical stretch and pathogenesis such as inflammation, disruption of cell junctions, and edema formation.
Mechanical stretch stimulates MSICs to increase transcellular ion exchange and subsequently generates VILI through inflammation and other pathogeneses mediated by MSICs signal-transmitting pathways. These findings make it possible to identify potential therapeutic targets for the prevention of lung injury through further exploration and more studies.
https://inplasy.com/inplasy-2024-10-0115/, identifier INPLASY2024100115.
呼吸机诱导性肺损伤（VILI）的发病机制仍有待阐明。机械通气过程中的机械力由肺内皮细胞、上皮细胞和免疫细胞中的机械敏感离子通道（MSICs）持续感知和传递。近年来，已表明MSICs与VILI有关。
从数据库建库至2024年3月，在PubMed、Cochrane图书馆、科学引文索引和ScienceDirect上进行了系统检索，并按照PRISMA指南进行综述。由两名作者独立评估潜在的合格研究。分析了研究特征、质量评估和潜在机制。
我们纳入了23项合格研究，其中大部分是在小鼠动物身上进行的。在细胞水平上，分别有52%和48%的实验是用人细胞或动物细胞进行的。未发现临床研究。报道最多的MSICs包括Piezo通道、瞬时受体电位通道、钾通道和牵张激活钠通道。Piezo1是近五年最受关注的通道。本研究发现，RhoA/ROCK1等信号通路可被周期性牵张激活的MSICs增强，其通过离子转运介导的炎症和免疫反应失调导致VILI。该综述表明MSICs在VILI发病机制中的新作用，尤其是作为机械牵张与炎症、细胞连接破坏和水肿形成等发病机制之间的信号传递纽带。
机械牵张刺激MSICs增加跨细胞离子交换，随后通过MSICs信号传递途径介导的炎症和其他发病机制产生VILI。这些发现使得通过进一步探索和更多研究来确定预防肺损伤的潜在治疗靶点成为可能。
https://inplasy.com/inplasy-2024-10-0115/，标识符INPLASY2024100115 。
