S1PR1型
特发性肺纤维化
博莱霉素
医学
肺纤维化
肺
纤维化
肺移植
癌症研究
鞘氨醇
免疫学
药理学
病理
内科学
受体
血管内皮生长因子A
血管内皮生长因子
化疗
血管内皮生长因子受体
作者
Mengyao Hao,Rong Fu,Jun Tai,Zhenhuan Tian,Xiaocong Yuan,Yang Chen,Mingjin Wang,Huimin Jiang,Ming Ji,Fangfang Lai,Nina Xue,Liping Bai,Yi‐Zhun Zhu,Xin Lv,Xiaoguang Chen,Jing Jin
标识
DOI:10.1016/j.apsb.2022.10.006
摘要
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with unclear etiology and limited treatment options. The median survival time for IPF patients is approximately 2–3 years and there is no effective intervention to treat IPF other than lung transplantation. As important components of lung tissue, endothelial cells (ECs) are associated with pulmonary diseases. However, the role of endothelial dysfunction in pulmonary fibrosis (PF) is incompletely understood. Sphingosine-1-phosphate receptor 1 (S1PR1) is a G protein-coupled receptor highly expressed in lung ECs. Its expression is markedly reduced in patients with IPF. Herein, we generated an endothelial-conditional S1pr1 knockout mouse model which exhibited inflammation and fibrosis with or without bleomycin (BLM) challenge. Selective activation of S1PR1 with an S1PR1 agonist, IMMH002, exerted a potent therapeutic effect in mice with bleomycin-induced fibrosis by protecting the integrity of the endothelial barrier. These results suggest that S1PR1 might be a promising drug target for IPF therapy.
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