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一个新的FGF15/19介导的肠心轴控制心脏缩

Samantha Morón-Ros¹, Albert Blasco-Roset¹, Artur Navarro-Gascon¹

¹Departament de Bioquímica i Biomedicina Molecular, Institut de Biomedicina (IBUB), Universitat de Barcelona and CIBER Fisiopatología de la Obesidad y Nutrición, Barcelona, Spain.

The Journal of pathology

|August 31, 2023

概括

来自肠道的纤维细胞生长因子15/19 (FGF15/19) 促进心脏缩. 缺乏FGF15的小鼠抵抗过度缩小,揭示了心脏病中的肠心轴.

科学领域:

内分泌学在内分泌学.
心血管生物学心血管生物学
代谢调节代谢调节代谢调节

背景情况:

纤维细胞生长因子15 (FGF15) 和其人体内生长因子FGF19是内分泌激素,由内皮肠细胞分泌.
虽然主要以向肝脏而闻名,但FGF15/19也影响骨肌肉和脂肪组织.
在人类心力衰竭患者中观察到高FGF19水平.

研究的目的:

为了研究内蛋白FGF15/19在心脏缩的发展中的作用.
阐明涉及FGF15/19从肠道到心脏的器官间信号通路.

主要方法:

使用的Fgf15-null小鼠接受了各种诱导高缩的刺激 (高脂肪饮食,异二醇,暴露于寒冷).
通过心脏重量/骨长度比率,心肌细胞面积和心房 natriuretic (Nppa) 水平评估心脏缩.
进行了心声回声和分析了与脂肪酸代谢相关的基因表达.
使用暴露于FGF19.19的分离心肌细胞进行了体外研究.

主要成果:

在病理条件下,Fgf15-null小鼠对心脏缩表现出抵抗力.
与野生类型对照相比,这些小鼠的心脏重量/骨长度比和心肌细胞大小减少.
FGF15缺乏改变了心脏脂肪酸代谢的基因表达.
直接使用FGF15/19诱导心脏缩并影响体外和体内代谢基因表达.

结论:

FGF15/19在肠心轴中起到关键的调解作用,促进心脏缩.
这种肠毒素在调节心肌脂肪酸代谢方面发挥着重要作用.
准FGF15/19通路可能为心脏缩提供治疗策略.

关键词:

联邦财政财政基金15/19/19 心脏过度缩小的心脏过度缩小内分泌系统内分泌系统心灵的心灵心灵的心灵心灵的心灵皮质皮质皮质皮质

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