CIRC RES:主动脉瓣发育发现新信号通路!

2017-12-23 MedSci MedSci原创

主动脉瓣膜疾病是一个细胞介导的过程,并且缺乏有效的药物治疗。C型钠尿肽(CNP)可以减少瓣膜间质细胞(VICs)的纤维生成和骨生成,其在狭窄的主动脉瓣膜中表达量降低,然而CNP信号通路是否在体内调节主动脉瓣生成尚属未知。本研究的目的旨在评估CNP信号通路的缺失是否会加快主动脉瓣膜疾病的进展。在猪主动脉瓣间质细胞中,CNP可以通过鸟苷酸环化酶钠尿肽受体2(NPR2)抑制病理分化。在Npr2+/-小鼠

主动脉瓣膜疾病是一个细胞介导的过程,并且缺乏有效的药物治疗。C型钠尿肽(CNP)可以减少瓣膜间质细胞(VICs)的纤维生成和骨生成,其在狭窄的主动脉瓣膜中表达量降低,然而CNP信号通路是否在体内调节主动脉瓣生成尚属未知。本研究的目的旨在评估CNP信号通路的缺失是否会加快主动脉瓣膜疾病的进展。在猪主动脉瓣间质细胞中,CNP可以通过鸟苷酸环化酶钠尿肽受体2(NPR2)抑制病理分化。在Npr2+/-小鼠的成纤维细胞中,纤维生成对CNP敏感,且年长的Npr2+/- 和Npr2+/-;Ldlr-/-转基因小鼠出现有心功能不全和心室纤维化,与同窝野生型对照小鼠相比,Npr2+/- 和Npr2+/-;Ldlr-/-转基因小鼠的主动脉瓣功能明显受损。9.4%的Npr2+/-小鼠出现有二叶主动脉瓣(BAV),并伴有主动脉瓣膜功能受损、增厚和钙化。此外,环磷酸鸟苷依赖性蛋白激酶(cGK)的活性在Npr2+/-小鼠的主动脉瓣膜中下调。研究结果显示,CNP/NPR2是主动脉瓣膜发育过程中的一个新的信号通路。原始出处:Mark C et al.Deficiency of Natriuretic Peptide

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    2017-12-25 neurowu
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    2017-12-24 三生有幸9135

    学习一下谢谢分享

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    2017-12-23 1e1b8538m79(暂无匿称)

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