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首页> 外文期刊>Journal of Molecular and Cellular Cardiology >Mst1 knockout enhances cardiomyocyte autophagic flux to alleviate angiotensin II-induced cardiac injury independent of angiotensin II receptors
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Mst1 knockout enhances cardiomyocyte autophagic flux to alleviate angiotensin II-induced cardiac injury independent of angiotensin II receptors

机译:MST1敲除增强心肌细胞自噬助体,以缓解血管紧张素II诱导的心脏损伤,与血管紧张素II受体无关

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摘要

Aims: Angiotension II (Ang II) plays a central role in the pathogenesis of renin-angiotensin-aldosterone system (RAAS)-induced heart failure. Mst1 exerts its function in cardiomyocytes subjected to pathological stimuli via inhibiting autophagy and aggravating apoptosis, but its role in RAAS-mediated cardiac injury is still unknown. Here, we aimed to determine whether cardiomyocyte-specific Mst1 knockout can alleviate Ang II-induced cardiac injury by improving cardiomyocyte autophagy and whether these functions depend on Ang II receptors.
机译:目的:血管紧张症II(Ang II)在肾素 - 血管紧张素 - 醛固酮系统(RAAS)引起的心力衰竭的发病机制中起着核心作用。 MST1通过抑制自噬和加重细胞凋亡,施加其在经过病理刺激的心肌细胞中的功能,但其在RAAS介导的心脏损伤中的作用仍然未知。 在这里,我们旨在通过改善心肌细胞自噬和这些功能是否依赖于Ang II受体,确定是否可以确定心肌细胞特异性MST1敲除是否可以缓解Ang II诱导的心损伤。

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