靶向P2X受体-败血症的最新进展

IF 2 Q3 IMMUNOLOGY
International Journal of Inflammation Pub Date : 2025-09-24 eCollection Date: 2025-01-01 DOI:10.1155/ijin/1083543
Lan Luo, Qian Zhao, Yunfen Tian, Meisha Sun, Mazhong Zhang, Bin Wang
{"title":"靶向P2X受体-败血症的最新进展","authors":"Lan Luo, Qian Zhao, Yunfen Tian, Meisha Sun, Mazhong Zhang, Bin Wang","doi":"10.1155/ijin/1083543","DOIUrl":null,"url":null,"abstract":"<p><p>Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Inflammation, as the main pathophysiological mechanism, runs through the whole course of sepsis. Notably, P2X receptors have the capacity to mediate inflammation, nerve signaling, and thrombosis, which underscores their pivotal role in the progression of sepsis. The goal of this study is to review the specific role of the P2X family in the pathogenesis of sepsis in various organs in light of currently available evidence.</p>","PeriodicalId":14004,"journal":{"name":"International Journal of Inflammation","volume":"2025 ","pages":"1083543"},"PeriodicalIF":2.0000,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12488317/pdf/","citationCount":"0","resultStr":"{\"title\":\"Targeting P2X Receptors-Current Progress in Sepsis.\",\"authors\":\"Lan Luo, Qian Zhao, Yunfen Tian, Meisha Sun, Mazhong Zhang, Bin Wang\",\"doi\":\"10.1155/ijin/1083543\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Inflammation, as the main pathophysiological mechanism, runs through the whole course of sepsis. Notably, P2X receptors have the capacity to mediate inflammation, nerve signaling, and thrombosis, which underscores their pivotal role in the progression of sepsis. The goal of this study is to review the specific role of the P2X family in the pathogenesis of sepsis in various organs in light of currently available evidence.</p>\",\"PeriodicalId\":14004,\"journal\":{\"name\":\"International Journal of Inflammation\",\"volume\":\"2025 \",\"pages\":\"1083543\"},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2025-09-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12488317/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Inflammation\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1155/ijin/1083543\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Inflammation","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1155/ijin/1083543","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

脓毒症被定义为由宿主对感染反应失调引起的危及生命的器官功能障碍。炎症作为主要的病理生理机制,贯穿于脓毒症的整个过程。值得注意的是,P2X受体具有介导炎症、神经信号传导和血栓形成的能力,这强调了它们在败血症进展中的关键作用。本研究的目的是根据现有证据回顾P2X家族在各器官脓毒症发病机制中的具体作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Targeting P2X Receptors-Current Progress in Sepsis.

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Inflammation, as the main pathophysiological mechanism, runs through the whole course of sepsis. Notably, P2X receptors have the capacity to mediate inflammation, nerve signaling, and thrombosis, which underscores their pivotal role in the progression of sepsis. The goal of this study is to review the specific role of the P2X family in the pathogenesis of sepsis in various organs in light of currently available evidence.

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
3.80
自引率
0.00%
发文量
16
审稿时长
16 weeks
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信