Circulation:抑制GSK3β可改善5型心律失常性右心室心肌病(ARVC)的心功能

2019-10-07 MedSci MedSci原创

心律失常性心肌病/心律失常性右心室心肌病(ARVC)是一种以心肌纤维脂肪替代为特征的遗传性心脏病,可导致心衰和心源性猝死。最具侵袭性的心律失常性心肌病/ARVC亚型为由MEM43基因p.S358L突变引起的5型ARVC(ARVC5)。近日Barthe等人在《循环》杂志上报道了ARVC5转基因小鼠模型的特征。Barthe等人建立了过表达野生型TMEM43或突变型TMEM43-S358L的转基因小鼠。

心律失常性心肌病/心律失常性右心室心肌病(ARVC)是一种以心肌纤维脂肪替代为特征的遗传性心脏病,可导致心衰和心源性猝死。最具侵袭性的心律失常性心肌病/ARVC亚型为由MEM43基因p.S358L突变引起的5型ARVC(ARVC5)。近日Barthe等人在《循环》杂志上报道了ARVC5转基因小鼠模型的特征。


Barthe等人建立了过表达野生型TMEM43或突变型TMEM43-S358L的转基因小鼠。


结果发现过表达TMEM43-S358L的转基因小鼠再现了人类疾病,并在年轻的时候死亡。突变型TMEM43引发心肌细胞死亡和严重的纤维脂肪替代。研究人员还发信息TMEM43定位于核膜上,与emerin(伊默菌素)和β-肌动蛋白互作。TMEM43-S358L表现部分异常定位于细胞质,与伊默菌素和β-肌动蛋白的互作减少,并可激活糖原合酶激酶-3β (GSK3β)。此外,研究人员还发现靶向心肌纤维化无任何效果,但过表达钙调磷酸酶拼接变体Aβ1可抑制GSK3β、改善心功能和存活。同样,用GSK3β抑制剂治疗TMEM43突变小鼠可改善心脏功能。最后,携带p.S358L突变的人诱导多能干细胞也显示出收缩功能障碍,抑制GSK3β后可恢复部分功能。


本研究表明TMEM43-S358L可导致持续的心肌细胞死亡和纤维脂肪替代。在TMEM43突变型小鼠中过表达钙调磷酸酶Aβ1或抑制GSK3β可提高心功能,并延长小鼠存活期。本研究为开发ARVC5的新治疗方法提供了方向。


原始出处:


Laura Padrón-Barthe, et al.Severe Cardiac Dysfunction and Death Caused by Arrhythmogenic Right Ventricular Cardiomyopathy Type 5 Are Improved by Inhibition of Glycogen Synthase Kinase-3β. Circulation. 2019;140:1188–1204


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    2019-12-02 anminleiryan
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    2020-09-12 luwei00
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