作者@article {Parpaleix470} ={本身{\ ' e留置权Parpaleix Val {\ ' e} rie Amsellem和阿玛尔Houssaini和部门阿比德和Marielle Breau伊丽莎白马科斯和Daigo Sawaki和马里昂Delcroix Rozenn Quarck和与{\ ' e}谎言美拉德和伊莎贝尔Couillin Bernhard Ryffel哔叽Adnot}, title ={作用受体1 / MyD88信号在开发及进展的肺动脉高压},体积={48}={2},页面= {470 - 483}= {2016},doi ={10.1183/13993003.01448 -2015},出版商={欧洲呼吸学会},文摘={肺动脉平滑肌细胞(PA-SMC)增殖和炎症肺动脉高血压(多环芳烃)的关键组件。188bet官网地址白介素(IL) 1β与IL - 1受体结合(R) 1,从而招募分子适配器骨髓分化主要响应蛋白88 (MyD88)(参与IL-1R1和toll样受体信号转导)和诱导IL - 1、IL - 6,通过核factor-κB激活肿瘤坏死factor-α合成。我们调查了IL-1R1 / MyD88通路在肺动脉高压的发病机制。标记IL-1R1和MyD88表达式主要PA-SMC疣状被发现在特发性肺动脉高压患者的肺,小鼠低氧诱导肺动脉高压和SM22-5-HTT +老鼠。海拔在肺IL-1βIL-1R1 MyD88和il - 6之前在小鼠缺氧肺动脉高压。IL-1R1 - / -, MyD88 - / -小鼠和控制由于IL-1R1拮抗剂anakinra是保护同样对缺氧性肺动脉高压和血管周的巨噬细胞招聘。Anakinra逆转肺动脉高压部分SM22-5-HTT +在monocrotaline-treated明显老鼠和老鼠。IL-1β-mediated鼠标PA-SMC增长的刺激是废除anakinra和缺席IL-1R1 - / -和MyD88 - / -小鼠。基因缺失局限于骨髓血统(M。lys-Cre MyD88fl / fl老鼠)降低肺动脉高压程度与控制,建议IL-1β-mediated PA-SMCs和巨噬细胞的影响。媒体的促生长效果受制于M1和M2巨噬细胞从M。lys-Cre MyD88fl / fl老鼠是衰减的。Pulmonary vessel remodelling and inflammation during pulmonary hypertension require IL-1R1/MyD88 signalling. Targeting the IL-1β/IL-1R1 pathway may hold promise for treating human PAH.The IL-1R1/MyD88 pathway is a treatment target for pulmonary arterial hypertension http://ow.ly/1Fpe3008RLs}, issn = {0903-1936}, URL = {//www.qdcxjkg.com/content/48/2/470}, eprint = {//www.qdcxjkg.com/content/48/2/470.full.pdf}, journal = {European Respiratory Journal} }