Department of Intensive Care Unit, Xiangya Hospital, Central South University, Changsha, China.
Department of Pulmonary and Critical Care Medicine, Center for Respiratory Diseases, China-Japan Friendship Hospital, National Clinical Research Center for Respiratory Diseases, Beijing, China.
Aging (Albany NY). 2020 Feb 15;12(4):3249-3265. doi: 10.18632/aging.102804.
The high mortality rate associated with acute respiratory distress syndrome (ARDS) is a major challenge for intensive care units. In the present study, we applied bioinformatics and animal models to identify core genes and potential corresponding pathways in ARDS.
Using bioinformatics analysis, IL-1β was identified as the core gene of ARDS. Cell experiments showed that up-regulation of IL-1β downregulates claudin18 to promote lung barrier function damage by regulating the IL-1β-HER2/HER3 axis, further promoting the development of ARDS. This was validated in the animal models.
IL-1β promotes the development of ARDS by regulating the IL-1β-HER2/HER3 axis. These findings deepen the understanding of the pathological mechanisms of ARDS.
Transcription data sets related to ARDS were subjected to differential expression gene analysis, functional enrichment analysis, and receiver operating characteristic curve analysis and, so as to identify core genes in ARDS. Cell experiments were used to further explore the effects of core genes on lung barrier function damage. Animal models were applied to validate the effects of core gene in mediating biological signal pathways in ARDS.
急性呼吸窘迫综合征（ARDS）的高死亡率是重症监护病房面临的主要挑战。本研究应用生物信息学和动物模型，鉴定 ARDS 的核心基因和潜在的相关通路。
通过生物信息学分析，鉴定出白细胞介素 1β（IL-1β）为 ARDS 的核心基因。细胞实验表明，IL-1β 的上调通过调节 IL-1β-HER2/HER3 轴下调 Claudin18 以促进肺屏障功能损伤，进一步促进 ARDS 的发展。这在动物模型中得到了验证。
IL-1β 通过调节 IL-1β-HER2/HER3 轴促进 ARDS 的发展。这些发现加深了对 ARDS 病理机制的理解。
对与 ARDS 相关的转录组数据集进行差异表达基因分析、功能富集分析、受试者工作特征曲线分析，以鉴定 ARDS 的核心基因。细胞实验进一步探讨了核心基因对肺屏障功能损伤的影响。应用动物模型验证核心基因在介导 ARDS 中生物信号通路的作用。
