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肌细胞周细胞在心肌缺血后会收缩血管。

Pericytes constrict blood vessels after myocardial ischemia.

机构信息

Department of Pathology, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.

Department of Radiology, Columbia University Medical Center, New York, NY, USA.

出版信息

J Mol Cell Cardiol. 2018 Mar;116:1-4. doi: 10.1016/j.yjmcc.2018.01.014. Epub 2018 Feb 3.

Abstract

No-reflow phenomenon is defined as the reduced blood flow after myocardial ischemia. If prolonged it leads to profound damages in the myocardium. The lack of a detailed knowledge about the cells mediating no-reflow restricts the design of effective therapies. Recently, O'Farrell et al. (2017) by using state-of-the-art technologies, including high-resolution confocal imaging in combination with myocardial ischemia/reperfusion mouse model, reveal that pericytes contribute to the no-reflow phenomenon post-ischemia in the heart. Strikingly, intravenous adenosine increased vascular diameter at pericyte site after cardiac ischemia. This study provides a novel therapeutic target to inhibit no-reflow phenomenon after myocardial ischemia.

摘要

无复流现象定义为心肌缺血后的血流减少。如果持续时间延长,会导致心肌严重损伤。由于对介导无复流的细胞缺乏详细了解,限制了有效治疗方法的设计。最近,O'Farrell 等人(2017 年)使用最先进的技术,包括高分辨率共聚焦成像结合心肌缺血/再灌注小鼠模型,揭示了周细胞在后缺血心脏的无复流现象中起作用。引人注目的是,心脏缺血后静脉内腺苷可增加周细胞部位的血管直径。这项研究为抑制心肌缺血后无复流现象提供了一个新的治疗靶点。

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