血管时钟系统产生血管收缩的内在昼夜节律

Q3 Medicine
Toshiro Saito
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引用次数: 9

摘要

许多心血管参数或冠状动脉疾病的发病率显示昼夜变化。这些昼夜时间差异可能归因于血管收缩能力的日变化。然而,产生血管收缩性昼夜变化的血管时钟系统的分子机制在很大程度上仍然未知。最近我们发现血管收缩存在内在的昼夜节律。血管平滑肌细胞(VSMC)中的时钟基因Rorα引起rho相关激酶2 (ROCK2)表达的昼夜振荡变化,从而诱导激动剂诱导的肌球蛋白轻链(MLC)磷酸化和肌丝Ca2+敏化的时间依赖性变化。本文就生物钟系统的分子基础和心血管时间生物学的最新研究进展作一综述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The vascular clock system generates the intrinsic circadian rhythm of vascular contractility
Many of the cardiovascular parameters or incidences of coronary artery diseases display circadian variations. These day/night time variances may be attributable to the diurnal change in vascular contractility. However, the molecular mechanism of the vascular clock system which generates the circadian variation of vascular contractility has remained largely unknown. Recently we found the existence of the intrinsic circadian rhythm in vascular contractility. A clock gene Rorα in vascular smooth muscle cells (VSMC) provokes the diurnal oscillatory change in the expression of Rho-associated kinase 2 (ROCK2), which induces the time-of-day-dependent variation in the agonist-induced phosphorylation of myosin light chain (MLC) and myofilament Ca2+ sensitization. In this review, we introduce our recent findings with reference to the molecular basis of the biological clock system and the current literature concerning cardiovascular chronobiology.
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来源期刊
Journal of Smooth Muscle Research
Journal of Smooth Muscle Research Biochemistry, Genetics and Molecular Biology-Physiology
CiteScore
2.30
自引率
0.00%
发文量
7
审稿时长
10 weeks
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