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长期偏差β-阿雷斯信号改善了扩展性心肌病的心脏结构和功能

David M Ryba¹, Jieli Li¹, Conrad L Cowan¹

¹From Department of Physiology and Biophysics and Center for Cardiovascular Research, University of Illinois at Chicago (D.M.R., J.L., B.R., B.M.W., R.J.S.); Department of Medicine, Division of Cardiology, University of Illinois at Chicago (B.M.W.); and Trevena, Inc. King of Prussia, PA (B.M.W.).

|January 21, 2017

概括

血管激素II受体的偏激激素在扩张性心肌病模型中改善了心脏功能,通过增强肌纤维反应能力. 这种方法可能为心力衰竭提供一种新的治疗策略.

科学领域:

心脏病学心脏病学
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

血管激素II受体的偏激激素通过肌纤维变化影响心脏收缩性.
扩张性心肌病症的特点是肌纤维纤维对的反应性降低.
贝塔-阿雷斯信号传递是改善家族扩张性心肌病中心脏功能的潜在目标.

研究的目的:

在家族扩张性心肌病的小鼠模型中,研究β-arrestin2偏向的血管新素II受体激动因子对肌纤维反应能力和心脏功能的影响.
阐明这些影响背后的信号机制,重点关注翻译后修饰和蛋白质相互作用.

主要方法:

在一个扩张性心肌病的小鼠模型 (Tm-E54K) 中,用β-arrestin 2偏差联结体 (TRV120067) 或洛萨坦治疗3个月.
通过心声学对心脏功能进行评估.
分析纤维捆中的肌纤维反应.
对翻译后修改的蛋白质组分析.
在体内和分离的肌细胞中评估信号通路.

主要成果:

与洛萨坦不同,TRV120067治疗改善了Tm-E54K小鼠的心脏结构和功能.
在接受TRV120067治疗的小鼠中,肌纤维反应显著增强.
观察到MLC2v和MYPT1/2的酸化增加,由ERK1/2-RSK3信号传递和肉瘤局部化的β-arrestin介导.

结论:

长期β-arrestin2偏向的血管增生素II受体激应是一种扩张性心肌病的潜在治疗策略.
这种方法通过增强肌纤维纤维反应能力来改善心脏功能.
贝塔-阿雷斯信号通路可能为治疗心力衰竭提供一种新的机制.

关键词:

TRV12002727 这是一本书.TRV12006767 这是一个很大的问题.有偏见的带.对于的敏感性萨尔科梅雷斯 (sarcomeres) 是一种类型的恶性毒素.

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