| 心律失常发病机制研究进展 |
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| 引用本文： | 杨宝峰,蔡本志.心律失常发病机制研究进展[J].国际药学研究杂志,2010,37(2):81-88. |
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| 作者姓名： | 杨宝峰 蔡本志 |
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| 作者单位： | 哈尔滨医科大学药学院药理学教研室,省部共建生物医药国家重点实验室培育基地,黑龙江哈尔滨,150081 |
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| 基金项目： | 国家重大基础研究发展计划"973计划"项目，国家自然科学基金重点项目，国家自然科学基金面上项目，国家自然科学基金中加国际合作项目 |
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| 摘 要： | 心律失常是心血管疾病常见的临床表现形式，尤其是室性心动过速、心室颤动等恶性心律失常，不但加重原有心脏疾病，还可诱发心源性猝死。目前抗心律失常药物的疗效并不十分理想，总有效率只有30%～60%。人们对心律失常作用机制的认识仍有限，因此，揭示心律失常发生的深层机制，寻找新的作用靶点是抗心律失常研究领域的重点、难点。近年人们发现心房特异性钾离子通道电流IKur、IKAch等参与了心房颤动，这使心房颤动治疗的研究向前推进一步。钙渗漏、缝隙连接蛋白及钙通道自身抗体在心律失常发生中发挥重要作用。这些发现为开发更有效的抗心律失常药物提供了理论基础。近年研究发现，一类调控基因的小分子RNA（microRNA,miRNA）在心血管疾病的发生、发展中起重要作用，特别是对心律失常及其引起的猝死起关键作用。miR-1、miR-133、miR-590等对心肌缺血、心肌梗死伴随的心律失常表现出明显调控作用。miRNA的生物学特性是同时对多个靶点具有调控作用，这使其具有成为理想抗心律失常靶点的潜力，为心律失常及猝死的防治带来希望。
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| 关 键 词： | 心律失常 离子通道 小分子RNA M3受体 心房颤动 缝隙连接蛋白 心肌梗死 AT1受体 溶血磷脂酰胆碱类 |
| 收稿时间： | 2010-3-12 |
| 修稿时间： | 2010-3-27 |
Advances in the study of arrhythmogenic mechanisms |
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| YANG Bao-feng,CAI Ben-zhi.Advances in the study of arrhythmogenic mechanisms[J].Foreign Medical Sciences(Section of Pharmarcy),2010,37(2):81-88. |
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| Authors: | YANG Bao-feng CAI Ben-zhi |
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| Affiliation: | （Department of Pharmacology, State-Province Key Laboratories of Biomedicine and Pharmaceutics, Harbin Medical University, Harbin 150081, China） |
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| Abstract: | Arrhythmia is a common complication of cardiovascular diseases and a risk factor for human health. Especially, ventricular tachycardia and ventricular fibrillation may not only exacerbate original heart diseases, but also cause cardiac sudden death which has been an important death reason in China. However, anti arrhythmic drugs nowadays cannot effectively treat these arrhythmias, with an efficiency of only 30%-60%, which indicates that our knowledge about arrhythmias is limited. Hence, to explore the potential mechanism, look for novel targets, and develop drugs with multiple channel action are the focus of the research direction. Recent studies displayed that the atrial-specific potassium channels such as IKur and IKAch were involved in atrial fibrillation, which provided a prospective target for atrial fibrillation treatment. Calcium leak, gap junction protein and autoantibody against ICaLchannel were shown to participate in arrhythmogenesis. These findings provided a theoretical basis for the development of more effective anti-arrhythmic drugs. Remarkably, as a kind of important RNA regulating gene expression, microRNA(miRNA) was shown to possess anti arrhythmic activities which may prevent cardiac sudden death. miR-1, miR-133 and miR-590 regulated the arrhythmia in various types of animal models. Because of the multiple-gene regulation actions of miRNA, it has the potential to be developed as novel anti-arrhythmic target. |
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| Keywords: | arrhythmia ion channels microRNA M3 receptor atrial fibrillation gap junction protein myocardial infarction AT1 receptor lysophosphatidylcholines |
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