冠状动脉痉挛的机制。

IF 3.2 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Kensuke Nishimiya, Jun Takahashi, Kazuma Oyama, Yasuharu Matsumoto, Satoshi Yasuda, Hiroaki Shimokawa
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引用次数: 1

摘要

最近的临床试验强调,经皮冠状动脉介入治疗在稳定型心绞痛患者中,除了最佳药物治疗外,还能提供有限的额外益处。这导致更多的关注冠状动脉血管舒张异常,无论阻塞性或非阻塞性动脉段。冠状动脉血管舒张受内皮、血管平滑肌细胞(VSMCs)、心肌代谢需求、自主神经系统和炎症等多种机制调控。多年来,人们已经建立了几种动物模型来探索冠状动脉痉挛的中心机制。本文综述了冠状血管痉挛机制的里程碑式研究,证明了rho激酶作为VSMC过度收缩的分子开关的核心作用,以及冠状动脉外膜炎症在VSMC中rho激酶上调的重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mechanisms of Coronary Artery Spasm.

Mechanisms of Coronary Artery Spasm.

Mechanisms of Coronary Artery Spasm.

Mechanisms of Coronary Artery Spasm.

Recent clinical trials have highlighted that percutaneous coronary intervention in patients with stable angina provides limited additional benefits on top of optimal medical therapy. This has led to much more attention being paid to coronary vasomotion abnormalities regardless of obstructive or non-obstructive arterial segments. Coronary vasomotion is regulated by multiple mechanisms that include the endothelium, vascular smooth muscle cells (VSMCs), myocardial metabolic demand, autonomic nervous system and inflammation. Over the years, several animal models have been developed to explore the central mechanism of coronary artery spasm. This review summarises the landmark studies on the mechanisms of coronary vasospasm demonstrating the central role of Rho-kinase as a molecular switch of VSMC hypercontraction and the important role of coronary adventitial inflammation for Rho-kinase upregulation in VSMCs.

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来源期刊
European Cardiology Review
European Cardiology Review CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
5.40
自引率
0.00%
发文量
23
审稿时长
12 weeks
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