RIPK1 inhibitor ameliorates pulmonary injury by modulating the function of neutrophils and vascular endothelial cells
文献类型：期刊论文
| 作者 | Yang, Tao3,4; Xiang, Cai-gui3,4; Wang, Xiao-han3,4; Li, Qing-qing4; Lei, Shu-yue3,4; Zhang, Kai-rong2; Ren, Jing1; Lu, Hui-min3,4; Feng, Chun-lan4; Tang, Wei3,4
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| 刊名 | CELL DEATH DISCOVERY
 |
| 出版日期 | 2024-03-23 |
| 卷号 | 10期号:1页码:12 |
| DOI | 10.1038/s41420-024-01921-8 |
| 通讯作者 | Tang, Wei(tangwei@simm.ac.cn) |
| 英文摘要 | Acute lung injury (ALI) is an acute and progressive hypoxic respiratory failure that could progress to acute respiratory distress syndrome (ARDS) with a high mortality rate, thus immediate medical attention and supportive care are necessary. The pathophysiology of ALI is characterized by the disruption of the alveolar-capillary barrier and activation of neutrophils, leading to lung tissue damage. The receptor-interacting protein kinase 1 (RIPK1) has emerged as a promising target for the treatment of multiple inflammatory diseases, but the role of RIPK1 in the ALI remains poorly understood. In this study, we aimed to figure out the pathological role of RIPK1 in ALI, especially in the pulmonary immune microenvironment involving neutrophils and endothelial cells. In vivo experiments showed that RIPK1 inhibitor protected against lipopolysaccharide (LPS)-induced lung injury in mouse models, with reduced neutrophils and monocytes infiltration in the lungs. Further studies demonstrated that, besides the inhibitory action on necroptosis, RIPK1 inhibitor directly suppressed reactive oxygen species (ROS) generation and inflammatory cytokines secretion from neutrophils. Furthermore, RIPK1 inhibition maintains the barrier function in TNF-alpha-primed vascular endothelial cells and prevents their activation induced by the supernatant from LPS-stimulated neutrophils. Mechanistically, the aforementioned effects of RIPK1 inhibitor are associated with the NF-kappa B signaling pathway, which is partially independent of necroptosis inhibition. These results provide new evidence that RIPK1 inhibitor directly regulates the function of neutrophils and endothelial cells, as well as interferes with the interactions between these two cell types, therefore contributing to a better understanding of RIPK1 in ALI and providing a potential avenue for future therapeutic interventions. |
| WOS关键词 | ACUTE LUNG INJURY ; INFLAMMATION ; PATHOGENESIS ; KINASES ; DEATH |
| 资助项目 | National Natural Science Foundation of China (National Science Foundation of China)[20JC1418000] ; Science and Technology Commission of Shanghai Municipality[82173822] ; National Natural Science Foundation of China |
| WOS研究方向 | Cell Biology |
| 语种 | 英语 |
| WOS记录号 | WOS:001189429300001 |
| 出版者 | SPRINGERNATURE |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/310339]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Tang, Wei |
| 作者单位 | 1.Nanjing Univ Chinese Med, Sch Chinese Mat Med, Nanjing 210000, Peoples R China 2.Nanchang Univ, Sch Pharmaceut Sci, Nanchang 330006, Peoples R China 3.Univ Chinese Acad Sci, Sch Pharm, Beijing 100049, Peoples R China 4.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Chem Biol, Shanghai 201203, Peoples R China |
| 推荐引用方式 GB/T 7714 | Yang, Tao,Xiang, Cai-gui,Wang, Xiao-han,et al. RIPK1 inhibitor ameliorates pulmonary injury by modulating the function of neutrophils and vascular endothelial cells[J]. CELL DEATH DISCOVERY,2024,10(1):12. |
| APA | Yang, Tao.,Xiang, Cai-gui.,Wang, Xiao-han.,Li, Qing-qing.,Lei, Shu-yue.,...&Tang, Wei.(2024).RIPK1 inhibitor ameliorates pulmonary injury by modulating the function of neutrophils and vascular endothelial cells.CELL DEATH DISCOVERY,10(1),12. |
| MLA | Yang, Tao,et al."RIPK1 inhibitor ameliorates pulmonary injury by modulating the function of neutrophils and vascular endothelial cells".CELL DEATH DISCOVERY 10.1(2024):12. |
入库方式： OAI收割
来源：上海药物研究所
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