首页> 美国卫生研究院文献>other >Mitochondrial Ultrastructural Alterations and Declined M2 Receptor Density Were Involved in Cardiac Dysfunction in Rats after Long Term Treatment with Autoantibodies against M2 Muscarinic Receptor
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Mitochondrial Ultrastructural Alterations and Declined M2 Receptor Density Were Involved in Cardiac Dysfunction in Rats after Long Term Treatment with Autoantibodies against M2 Muscarinic Receptor

机译:长期用抗M2毒蕈碱受体自身抗体治疗的大鼠心脏功能异常涉及线粒体超微结构改变和M2受体密度下降。

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摘要

BackgroundPrevious studies showed that autoantibodies (M2-AA) against the second extracellular loop of M2 muscarinic receptor (M2AChR-el2) from dilated cardiomyopathy (DCM) serum could induce DCM-like morphological changes in mice hearts. However, the effects of M2-AA on the cardiac function during the process of DCM and the potential mechanisms are not fully known. The present study was designed to dynamically observe the cardiac function, mitochondrial changes, and M2 receptor binding characteristics in rats long-term stimulated with M2-AA in vivo.
机译:背景先前的研究表明,针对扩张型心肌病(DCM)血清中M2毒蕈碱受体(M2AChR-el2)的第二个细胞外环的自身抗体(M2-AA)可以诱导小鼠心脏中的DCM样形态变化。但是,M2-AA对DCM过程中心脏功能的影响及其潜在机制尚不完全清楚。本研究旨在动态观察长期受体内M2-AA刺激的大鼠的心脏功能,线粒体变化和M2受体结合特征。

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