• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

钾通道与血管增殖。

Potassium channels and vascular proliferation.

作者信息

Neylon Craig B

机构信息

Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Victoria 3010, Australia.

出版信息

Vascul Pharmacol. 2002 Jan;38(1):35-41. doi: 10.1016/s1537-1891(02)00124-6.

DOI:10.1016/s1537-1891(02)00124-6
PMID:12378821
Abstract

Potassium channels are currently the focus of much attention because of their recently discovered role in the regulation of vascular smooth muscle growth. Dramatic alterations in the expression and activity of K+ channels causing marked changes in the cell's electrical properties accompany enhanced growth of smooth muscle cells (SMCs). These findings indicate that alterations in K+ channel function are important for SMC proliferation. However, the mechanisms by which changes in K+ channel activity influence cellular growth pathways are poorly understood. The emergent electrical properties caused by modulation of K+ channels are associated with marked differences in the spatial and temporal organization of Ca2+ signaling. Thus, changes in K+ channel function may represent a universal mechanism by which Ca2+ signals are targeted towards activation of gene expression and cell growth. As enhanced growth of smooth muscle underlies many cardiovascular diseases and clinical pathologies, the identification of an important role for K+ channels in SMC proliferation indicates a new source of therapeutic targets to regulate proliferative vascular disorders.

摘要

钾通道目前备受关注,因为它们最近被发现参与调节血管平滑肌生长。随着平滑肌细胞(SMC)生长增强,钾通道表达和活性的显著改变会导致细胞电特性发生明显变化。这些发现表明,钾通道功能的改变对SMC增殖很重要。然而,钾通道活性变化影响细胞生长途径的机制却知之甚少。钾通道调节引起的新出现的电特性与Ca2+信号在空间和时间组织上的显著差异有关。因此,钾通道功能的变化可能代表一种普遍机制,通过该机制Ca2+信号靶向激活基因表达和细胞生长。由于平滑肌生长增强是许多心血管疾病和临床病理的基础,钾通道在SMC增殖中重要作用的确定为调节增殖性血管疾病指明了新的治疗靶点来源。

相似文献

1
Potassium channels and vascular proliferation.钾通道与血管增殖。
Vascul Pharmacol. 2002 Jan;38(1):35-41. doi: 10.1016/s1537-1891(02)00124-6.
2
Ca2+ channels, ryanodine receptors and Ca(2+)-activated K+ channels: a functional unit for regulating arterial tone.钙离子通道、兰尼碱受体与钙激活钾通道:调节动脉张力的功能单元
Acta Physiol Scand. 1998 Dec;164(4):577-87. doi: 10.1046/j.1365-201X.1998.00462.x.
3
Detection and implications of potassium channel alterations.钾通道改变的检测及其影响
Vascul Pharmacol. 2002 Jan;38(1):3-12. doi: 10.1016/s1537-1891(02)00121-0.
4
Physiological roles of K+ channels in vascular smooth muscle cells.钾离子通道在血管平滑肌细胞中的生理作用。
J Smooth Muscle Res. 2008 Apr;44(2):65-81. doi: 10.1540/jsmr.44.65.
5
Changes in the expression and function of arterial potassium channels during hypertension.高血压期间动脉钾通道表达和功能的变化。
Vascul Pharmacol. 2002 Jan;38(1):13-23. doi: 10.1016/s1537-1891(02)00122-2.
6
Potassium channel modulation: a new drug principle for regulation of smooth muscle contractility. Studies on isolated airways and arteries.钾通道调节:一种调节平滑肌收缩性的新药理原则。对离体气道和动脉的研究。
Dan Med Bull. 1996 Dec;43(5):429-47.
7
Mechanisms of cellular synchronization in the vascular wall. Mechanisms of vasomotion.血管壁细胞同步化机制。血管运动机制。
Dan Med Bull. 2010 Oct;57(10):B4191.
8
Alteration of arterial smooth muscle potassium channel composition and BKCa current modulation in hypertension.高血压患者动脉平滑肌钾通道组成的改变及大电导钙激活钾电流的调节
Eur J Pharmacol. 2005 May 9;514(2-3):111-9. doi: 10.1016/j.ejphar.2005.03.032.
9
Sarcoplasmic reticulum and membrane currents.肌浆网与膜电流
Novartis Found Symp. 2002;246:189-203; discussion 203-7, 221-7.
10
Role of K+ channels in pulmonary hypertension.钾离子通道在肺动脉高压中的作用。
Vascul Pharmacol. 2002 Jan;38(1):25-33. doi: 10.1016/s1537-1891(02)00123-4.

引用本文的文献

1
Functional cooperation between IK and TRPC1 channels regulates serum-induced vascular smooth muscle cell proliferation via mediating Ca influx and ERK1/2 activation.IK 和 TRPC1 通道的功能合作通过调节 Ca2+内流和 ERK1/2 激活来调节血清诱导的血管平滑肌细胞增殖。
Cell Prolif. 2023 Apr;56(4):e13385. doi: 10.1111/cpr.13385. Epub 2022 Dec 23.
2
The Calcium Signaling Mechanisms in Arterial Smooth Muscle and Endothelial Cells.动脉平滑肌和内皮细胞中的钙信号机制。
Compr Physiol. 2021 Apr 1;11(2):1831-1869. doi: 10.1002/cphy.c200030.
3
The mechanism of ions in pulmonary hypertension.
离子在肺动脉高压中的作用机制。
Pulm Circ. 2021 Jan 27;11(1):2045894020987948. doi: 10.1177/2045894020987948. eCollection 2021 Jan-Mar.
4
Myocardin and Kv1 Channels: A Paradigm Shift in Treating Vascular Smooth Muscle Cell-Related Proliferative Disease?心肌素与钾离子通道 Kv1:治疗血管平滑肌细胞相关增殖性疾病的范式转变?
Arterioscler Thromb Vasc Biol. 2019 Dec;39(12):2454-2456. doi: 10.1161/ATVBAHA.119.313531. Epub 2019 Nov 26.
5
Iron Oxide Nanoparticles Stimulates Extra-Cellular Matrix Production in Cellular Spheroids.氧化铁纳米颗粒刺激细胞球体中的细胞外基质产生。
Bioengineering (Basel). 2017 Jan 21;4(1):4. doi: 10.3390/bioengineering4010004.
6
Potassium Channels in Regulation of Vascular Smooth Muscle Contraction and Growth.钾通道在血管平滑肌收缩和生长调节中的作用
Adv Pharmacol. 2017;78:89-144. doi: 10.1016/bs.apha.2016.07.001. Epub 2016 Aug 17.
7
The roles of K(+) channels in cancer.钾离子通道在癌症中的作用。
Nat Rev Cancer. 2014 Jan;14(1):39-48. doi: 10.1038/nrc3635. Epub 2013 Dec 12.
8
The intermediate conductance calcium-activated potassium channel KCa3.1 regulates vascular smooth muscle cell proliferation via controlling calcium-dependent signaling.中等电导钙激活钾通道 KCa3.1 通过控制钙依赖性信号转导调节血管平滑肌细胞增殖。
J Biol Chem. 2013 May 31;288(22):15843-53. doi: 10.1074/jbc.M112.427187. Epub 2013 Apr 22.
9
Characterisation of K+ channels in human fetoplacental vascular smooth muscle cells.人胎盘中血管平滑肌细胞钾离子通道的特性。
PLoS One. 2013;8(2):e57451. doi: 10.1371/journal.pone.0057451. Epub 2013 Feb 21.
10
Fluoxetine protects against big endothelin-1 induced anti-apoptosis by rescuing Kv1.5 channels in human pulmonary arterial smooth muscle cells.氟西汀通过挽救人肺动脉平滑肌细胞中的 Kv1.5 通道来防止大内皮素-1 诱导的抗细胞凋亡。
Yonsei Med J. 2012 Jul 1;53(4):842-8. doi: 10.3349/ymj.2012.53.4.842.