心脏再生导致浦肯野纤维网和心室传导发生改变

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Nature cardiovascular research Pub Date : 2024-11-12 DOI:10.1038/s44161-024-00549-2
{"title":"心脏再生导致浦肯野纤维网和心室传导发生改变","authors":"","doi":"10.1038/s44161-024-00549-2","DOIUrl":null,"url":null,"abstract":"In newborn mice, after a neonatal cardiac infarction, cells derived from the ventricular trabeculae participate in the repair of the contractile myocardium, but this process results in excessive production of immature Purkinje fibers that form a hyperplastic network and lead to altered ventricular conduction.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 11","pages":"1272-1273"},"PeriodicalIF":9.4000,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Cardiac regeneration leads to altered Purkinje fiber network and ventricular conduction\",\"authors\":\"\",\"doi\":\"10.1038/s44161-024-00549-2\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"In newborn mice, after a neonatal cardiac infarction, cells derived from the ventricular trabeculae participate in the repair of the contractile myocardium, but this process results in excessive production of immature Purkinje fibers that form a hyperplastic network and lead to altered ventricular conduction.\",\"PeriodicalId\":74245,\"journal\":{\"name\":\"Nature cardiovascular research\",\"volume\":\"3 11\",\"pages\":\"1272-1273\"},\"PeriodicalIF\":9.4000,\"publicationDate\":\"2024-11-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature cardiovascular research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.nature.com/articles/s44161-024-00549-2\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature cardiovascular research","FirstCategoryId":"1085","ListUrlMain":"https://www.nature.com/articles/s44161-024-00549-2","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0

摘要

在新生小鼠中,新生儿心肌梗死后,来自心室小梁的细胞参与了收缩心肌的修复,但这一过程会导致过量产生未成熟的浦肯野纤维,形成增生网络,并导致心室传导发生改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

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
Cardiac regeneration leads to altered Purkinje fiber network and ventricular conduction
In newborn mice, after a neonatal cardiac infarction, cells derived from the ventricular trabeculae participate in the repair of the contractile myocardium, but this process results in excessive production of immature Purkinje fibers that form a hyperplastic network and lead to altered ventricular conduction.
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
CiteScore
5.70
自引率
0.00%
发文量
0
期刊最新文献
Implications and limitations of the CLEAR-SYNERGY trial for the use of low-dose colchicine in cardiovascular disease. Discovering and targeting mitochondrial loss in NOTCH1-related aortic aneurysm. Mitochondrial NAD+ deficiency in vascular smooth muscle impairs collagen III turnover to trigger thoracic and abdominal aortic aneurysm. Mitochondrial NAD+ transporter SLC25A51 linked to human aortic disease. The clinical promise of 18F-flurpiridaz PET imaging heralds a new frontier in the diagnosis and management of coronary artery disease
×
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