内皮TRPV4通道和血管扩张剂反应性。

4区 生物学 Q4 Biochemistry, Genetics and Molecular Biology Current topics in membranes Pub Date : 2020-01-01 DOI:10.1016/bs.ctm.2020.01.007
Yen-Lin Chen, Swapnil K Sonkusare
{"title":"内皮TRPV4通道和血管扩张剂反应性。","authors":"Yen-Lin Chen,&nbsp;Swapnil K Sonkusare","doi":"10.1016/bs.ctm.2020.01.007","DOIUrl":null,"url":null,"abstract":"<p><p>Transient receptor potential vanilloid 4 (TRPV4) ion channels on the endothelial cell membrane are widely regarded as a crucial Ca<sup>2+</sup> influx pathway that promotes endothelium-dependent vasodilation. The downstream vasodilatory targets of endothelial TRPV4 channels vary among different vascular beds, potentially contributing to endothelial cell heterogeneity. Although numerous studies have examined the role of endothelial TRPV4 channels using specific pharmacological tools over the past decade, their physiological significance remains unclear, mainly due to a lack of endothelium-specific knockouts. Moreover, the loss of endothelium-dependent vasodilation is a significant contributor to vascular dysfunction in cardiovascular disease. The activity of endothelial TRPV4 channels is impaired in cardiovascular disease; therefore, strategies targeting the mechanisms that reduce endothelial TRPV4 channel activity may restore vascular function and provide therapeutic benefit. In this chapter, we discuss endothelial TRPV4 channel-dependent signaling mechanisms, the heterogeneity in endogenous activators and targets of endothelial TRPV4 channels, and the role of endothelial TRPV4 channels in the pathogenesis of cardiovascular diseases. We also discuss potentially interesting future research directions that may provide novel insights into the physiological and pathological roles of endothelial TRPV4 channels.</p>","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"85 ","pages":"89-117"},"PeriodicalIF":0.0000,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/bs.ctm.2020.01.007","citationCount":"20","resultStr":"{\"title\":\"Endothelial TRPV4 channels and vasodilator reactivity.\",\"authors\":\"Yen-Lin Chen,&nbsp;Swapnil K Sonkusare\",\"doi\":\"10.1016/bs.ctm.2020.01.007\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Transient receptor potential vanilloid 4 (TRPV4) ion channels on the endothelial cell membrane are widely regarded as a crucial Ca<sup>2+</sup> influx pathway that promotes endothelium-dependent vasodilation. The downstream vasodilatory targets of endothelial TRPV4 channels vary among different vascular beds, potentially contributing to endothelial cell heterogeneity. Although numerous studies have examined the role of endothelial TRPV4 channels using specific pharmacological tools over the past decade, their physiological significance remains unclear, mainly due to a lack of endothelium-specific knockouts. Moreover, the loss of endothelium-dependent vasodilation is a significant contributor to vascular dysfunction in cardiovascular disease. The activity of endothelial TRPV4 channels is impaired in cardiovascular disease; therefore, strategies targeting the mechanisms that reduce endothelial TRPV4 channel activity may restore vascular function and provide therapeutic benefit. In this chapter, we discuss endothelial TRPV4 channel-dependent signaling mechanisms, the heterogeneity in endogenous activators and targets of endothelial TRPV4 channels, and the role of endothelial TRPV4 channels in the pathogenesis of cardiovascular diseases. We also discuss potentially interesting future research directions that may provide novel insights into the physiological and pathological roles of endothelial TRPV4 channels.</p>\",\"PeriodicalId\":11029,\"journal\":{\"name\":\"Current topics in membranes\",\"volume\":\"85 \",\"pages\":\"89-117\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/bs.ctm.2020.01.007\",\"citationCount\":\"20\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current topics in membranes\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1016/bs.ctm.2020.01.007\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current topics in membranes","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/bs.ctm.2020.01.007","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 20

摘要

内皮细胞膜上的瞬时受体电位香草样蛋白4 (TRPV4)离子通道被广泛认为是促进内皮依赖性血管舒张的关键Ca2+内流途径。内皮细胞TRPV4通道的下游血管舒张靶点在不同的血管床中存在差异,这可能导致内皮细胞的异质性。尽管在过去的十年中,许多研究使用特定的药理学工具检查了内皮TRPV4通道的作用,但其生理意义尚不清楚,主要是由于缺乏内皮特异性敲除。此外,内皮依赖性血管舒张功能的丧失是心血管疾病中血管功能障碍的重要因素。内皮细胞TRPV4通道活性在心血管疾病中受损;因此,针对降低内皮TRPV4通道活性的机制的策略可能会恢复血管功能并提供治疗益处。在本章中,我们将讨论内皮TRPV4通道依赖的信号机制,内皮TRPV4通道内源性激活剂和靶点的异质性,以及内皮TRPV4通道在心血管疾病发病机制中的作用。我们还讨论了未来可能有趣的研究方向,这些方向可能为内皮细胞TRPV4通道的生理和病理作用提供新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Endothelial TRPV4 channels and vasodilator reactivity.

Transient receptor potential vanilloid 4 (TRPV4) ion channels on the endothelial cell membrane are widely regarded as a crucial Ca2+ influx pathway that promotes endothelium-dependent vasodilation. The downstream vasodilatory targets of endothelial TRPV4 channels vary among different vascular beds, potentially contributing to endothelial cell heterogeneity. Although numerous studies have examined the role of endothelial TRPV4 channels using specific pharmacological tools over the past decade, their physiological significance remains unclear, mainly due to a lack of endothelium-specific knockouts. Moreover, the loss of endothelium-dependent vasodilation is a significant contributor to vascular dysfunction in cardiovascular disease. The activity of endothelial TRPV4 channels is impaired in cardiovascular disease; therefore, strategies targeting the mechanisms that reduce endothelial TRPV4 channel activity may restore vascular function and provide therapeutic benefit. In this chapter, we discuss endothelial TRPV4 channel-dependent signaling mechanisms, the heterogeneity in endogenous activators and targets of endothelial TRPV4 channels, and the role of endothelial TRPV4 channels in the pathogenesis of cardiovascular diseases. We also discuss potentially interesting future research directions that may provide novel insights into the physiological and pathological roles of endothelial TRPV4 channels.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Current topics in membranes
Current topics in membranes 生物-生化与分子生物学
CiteScore
3.50
自引率
0.00%
发文量
10
审稿时长
>12 weeks
期刊介绍: Current Topics in Membranes provides a systematic, comprehensive, and rigorous approach to specific topics relevant to the study of cellular membranes. Each volume is a guest edited compendium of membrane biology.
期刊最新文献
How has the evolution of our understanding of the compartmentalization of sphingolipid biosynthesis over the past 30 years altered our view of the evolution of the pathway? Endocytosis in malaria parasites: An ultrastructural perspective of membrane interplay in a unique infection model. Impact of coat protein on evolution of ilarviruses. Lysosomal membrane contact sites: Integrative hubs for cellular communication and homeostasis. Preface.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1