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中华危重症医学杂志(电子版) ›› 2023, Vol. 16 ›› Issue (05) : 409 -413. doi: 10.3877/cma.j.issn.1674-6880.2023.05.011

综述

"炎症-RhoA/ROCK通路-微管解聚"正反馈回路在急性肺损伤/急性呼吸窘迫综合征中的作用机制
朱鹏, 雍文兴, 吴亚娜, 徐倩, 张录梅, 郝国雄, 刘瑜, 张志明()   
  1. 100072 北京,北京市丰台中西医结合医院消化(内分泌)科
    730000 兰州,甘肃中医药大学附属医院急诊科
    730000 兰州,甘肃中医药大学中医临床学院
    730050 兰州,甘肃省中医院名医工作站
  • 收稿日期:2022-10-18 出版日期:2023-10-31
  • 通信作者: 张志明
  • 基金资助:
    高端人才承担省级科技计划项目("长江学者奖励计划"特聘教授)(甘科计〔2022〕20号-9); 甘肃省科技计划重大专项(甘科计〔2022〕1号-25); 甘肃省中医药管理局科研项目(GZKP-2020-8); 兰州市人才创新创业项目(2021-RC-80); 兰州市科技发展计划项目(2020-XG-29)
  • Received:2022-10-18 Published:2023-10-31
引用本文:

朱鹏, 雍文兴, 吴亚娜, 徐倩, 张录梅, 郝国雄, 刘瑜, 张志明. "炎症-RhoA/ROCK通路-微管解聚"正反馈回路在急性肺损伤/急性呼吸窘迫综合征中的作用机制[J/OL]. 中华危重症医学杂志(电子版), 2023, 16(05): 409-413.

急性肺损伤(acute lung injury,ALI)/急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)是一种由肺泡-毛细血管膜通透性增加引起的低氧性呼吸功能不全等肺部炎症综合征[1],以严重的低氧血症、急性及进行性呼吸功能不全、肺水肿和呼吸衰竭等为主要临床特征[2],具有病因及发病机制复杂、病死率高等特点[3]。ALI/ARDS已有大量的研究,但其病因机制仍未完全阐明,亦未发现较为满意的治疗措施,故病死率仍高达30% ~ 40%[4],进一步探究ALI/ARDS发生发展的机制以便寻求新的治疗靶点尤为重要。目前已探明的ALI/ARDS病理生理及其机制包括炎症反应、细胞损伤、细胞凋亡或自噬、血栓形成等所致的肺血管内皮细胞和肺泡上皮细胞损伤[5]。尤其是"炎症-Ras同源基因家族成员A(Ras homolog gene family, member A,RhoA)/Rho激酶(Rho-associated kinase,ROCK)通路-微管解聚"正反馈回路,促进了内皮细胞骨架肌动蛋白微管解聚,加剧了肺血管内皮细胞收缩、通透性及损伤程度,在ALI/ARDS的发生发展中起到了关键作用。因此本研究就"炎症-RhoA/ROCK通路-微管解聚"与肺损伤发病机制间的关系进行综合探讨并为临床治疗提供新的思路。

图1 "炎症-RhoA/ROCK通路-微管解聚"导致屏障功能破坏的机制图注:RhoA. Ras同源基因家族成员A;ROCK. Rho激酶;LPS.脂多糖;IL-6.白细胞介素6;TNF-α.肿瘤坏死因子α;GEF.鸟嘌呤核苷酸交换因子;GTP.三磷酸鸟苷;MAP-4.微管关联蛋白4
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