静脉血栓的靶向治疗:实验性的奢侈还是切实的未来?

О. Y. Porembskaya, E. Starikova, К. V. Lobastov, D. T. Mammedova, L. Laberko, V. Kravchuk, S. Saiganov
{"title":"静脉血栓的靶向治疗:实验性的奢侈还是切实的未来?","authors":"О. Y. Porembskaya, E. Starikova, К. V. Lobastov, D. T. Mammedova, L. Laberko, V. Kravchuk, S. Saiganov","doi":"10.33920/med-15-2204-05","DOIUrl":null,"url":null,"abstract":"Anticoagulant therapy is considered to be a treatment and prophylaxis standard for venous thrombosis (VT). Despite the high efficacy and safety of modern anticoagulants, bleeding as the side effect remains a prominent unresolved problem that can limit their use. As interrelation between immune system and coagulation is the basis of immunothrombosis, immunosuppression could be considered an alternative in the target therapy for venous thrombosis. Endothelial activation due to the blood stasis and vein wall hypoxia together with proinflammatory mediators promote essential conditions for venous thrombosis. The key points of this process are also the platelets and leukocytes activation and neutrophil extracellular traps secretion. Inhibition of intercellular interactions by the adhesion and signal molecules deletion (P-selectins, galectins, HMGB1) can fully prevent thrombosis or significantly reduce the thrombus. The same effect is observed when platelets function is suppressed by GPIbα transformation, CLEC-2 deletion or von Willebrand factor deficiency. Neutropenia contributes to a change in the thrombus structure and density, and less often prevents its formation. In addition, one of the options for the VT prevention in the experiment is the introduction of resorption mediators, which are secreted by effector cells in the process of thrombosis resolution. Target therapy appears to be a promising method based on key links in the VT pathogenesis, which may allow avoiding typical complications of anticoagulant therapy.","PeriodicalId":437500,"journal":{"name":"Hirurg (Surgeon)","volume":"10 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2022-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Target therapy for venous thrombosis: experimental extravagance or tangible future?\",\"authors\":\"О. Y. Porembskaya, E. Starikova, К. V. Lobastov, D. T. Mammedova, L. Laberko, V. Kravchuk, S. Saiganov\",\"doi\":\"10.33920/med-15-2204-05\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Anticoagulant therapy is considered to be a treatment and prophylaxis standard for venous thrombosis (VT). Despite the high efficacy and safety of modern anticoagulants, bleeding as the side effect remains a prominent unresolved problem that can limit their use. As interrelation between immune system and coagulation is the basis of immunothrombosis, immunosuppression could be considered an alternative in the target therapy for venous thrombosis. Endothelial activation due to the blood stasis and vein wall hypoxia together with proinflammatory mediators promote essential conditions for venous thrombosis. The key points of this process are also the platelets and leukocytes activation and neutrophil extracellular traps secretion. Inhibition of intercellular interactions by the adhesion and signal molecules deletion (P-selectins, galectins, HMGB1) can fully prevent thrombosis or significantly reduce the thrombus. The same effect is observed when platelets function is suppressed by GPIbα transformation, CLEC-2 deletion or von Willebrand factor deficiency. Neutropenia contributes to a change in the thrombus structure and density, and less often prevents its formation. In addition, one of the options for the VT prevention in the experiment is the introduction of resorption mediators, which are secreted by effector cells in the process of thrombosis resolution. Target therapy appears to be a promising method based on key links in the VT pathogenesis, which may allow avoiding typical complications of anticoagulant therapy.\",\"PeriodicalId\":437500,\"journal\":{\"name\":\"Hirurg (Surgeon)\",\"volume\":\"10 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-07-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Hirurg (Surgeon)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.33920/med-15-2204-05\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Hirurg (Surgeon)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.33920/med-15-2204-05","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1

摘要

抗凝治疗被认为是静脉血栓形成(VT)的治疗和预防标准。尽管现代抗凝剂具有很高的疗效和安全性,但出血作为副作用仍然是一个突出的未解决的问题,限制了它们的使用。免疫系统与凝血之间的相互关系是免疫血栓形成的基础,免疫抑制可作为静脉血栓形成的一种靶向治疗方法。由于血瘀和静脉壁缺氧引起的内皮活化与促炎介质一起促进静脉血栓形成的必要条件。这一过程的关键也是血小板和白细胞的活化和中性粒细胞胞外陷阱的分泌。通过粘附和信号分子(p -选择素、凝集素、HMGB1)的缺失抑制细胞间相互作用,可以充分预防血栓形成或显著减少血栓形成。当血小板功能被GPIbα转化、CLEC-2缺失或血管性血液病因子缺乏抑制时,也观察到同样的效果。中性粒细胞减少有助于改变血栓的结构和密度,很少阻止血栓的形成。此外,本实验中预防VT的一种选择是引入吸收介质,它是由效应细胞在血栓溶解过程中分泌的。靶向治疗似乎是一种很有前途的方法,它基于VT发病机制的关键环节,可以避免抗凝治疗的典型并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Target therapy for venous thrombosis: experimental extravagance or tangible future?
Anticoagulant therapy is considered to be a treatment and prophylaxis standard for venous thrombosis (VT). Despite the high efficacy and safety of modern anticoagulants, bleeding as the side effect remains a prominent unresolved problem that can limit their use. As interrelation between immune system and coagulation is the basis of immunothrombosis, immunosuppression could be considered an alternative in the target therapy for venous thrombosis. Endothelial activation due to the blood stasis and vein wall hypoxia together with proinflammatory mediators promote essential conditions for venous thrombosis. The key points of this process are also the platelets and leukocytes activation and neutrophil extracellular traps secretion. Inhibition of intercellular interactions by the adhesion and signal molecules deletion (P-selectins, galectins, HMGB1) can fully prevent thrombosis or significantly reduce the thrombus. The same effect is observed when platelets function is suppressed by GPIbα transformation, CLEC-2 deletion or von Willebrand factor deficiency. Neutropenia contributes to a change in the thrombus structure and density, and less often prevents its formation. In addition, one of the options for the VT prevention in the experiment is the introduction of resorption mediators, which are secreted by effector cells in the process of thrombosis resolution. Target therapy appears to be a promising method based on key links in the VT pathogenesis, which may allow avoiding typical complications of anticoagulant therapy.
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
自引率
0.00%
发文量
0
×
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