内皮细胞衍生的微颗粒免疫表型受损:糖尿病相关状态与心血管并发症风险之间的缺失环节?

Alex, er E. Berezin
{"title":"内皮细胞衍生的微颗粒免疫表型受损:糖尿病相关状态与心血管并发症风险之间的缺失环节?","authors":"Alex, er E. Berezin","doi":"10.4172/2153-0602.1000195","DOIUrl":null,"url":null,"abstract":"Type two diabetes mellitus (T2DM) remains a leading contributor to cardiovascular (CV) mortality worldwide. Although obese and metabolic syndrome are discussed key factors contributing a higher risk of T2DM, the exact molecular mechanisms underlying to the progression of dysmetabolic states are still not completely clear. There is large body of evidence regarding endothelial dysfunction as a key player in increasing CV risk and that vascular damage in the dysmetabolic patients might mediate through an imbalance between various populations of micro particle (MP). The short commentary is discussed a role of impaired ratio between apoptotic MPs and activated MPs derived from endothelial cells that was recognized as “impaired phenotype” of endothelial cell-derived MPs. It has considered the causality epigenetic reprogramming, metabolic disorders, inflammation, and oxidative stress in forming of “impaired phenotype” of MPs. The incorporation of measurement of the endothelial cell-derived MP number into a conventional CV risk factor model aimed improving of risk stratification of the dysmetabolic patients with high probability of CV disease is discussed.","PeriodicalId":15630,"journal":{"name":"Journal of Data Mining in Genomics & Proteomics","volume":"22 1","pages":"1-3"},"PeriodicalIF":0.0000,"publicationDate":"2016-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"35","resultStr":"{\"title\":\"Impaired Immune Phenotype of Endothelial Cell-derived Micro Particles: The Missing Link between Diabetes-related States and Risk of Cardiovascular Complications?\",\"authors\":\"Alex, er E. Berezin\",\"doi\":\"10.4172/2153-0602.1000195\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Type two diabetes mellitus (T2DM) remains a leading contributor to cardiovascular (CV) mortality worldwide. Although obese and metabolic syndrome are discussed key factors contributing a higher risk of T2DM, the exact molecular mechanisms underlying to the progression of dysmetabolic states are still not completely clear. There is large body of evidence regarding endothelial dysfunction as a key player in increasing CV risk and that vascular damage in the dysmetabolic patients might mediate through an imbalance between various populations of micro particle (MP). The short commentary is discussed a role of impaired ratio between apoptotic MPs and activated MPs derived from endothelial cells that was recognized as “impaired phenotype” of endothelial cell-derived MPs. It has considered the causality epigenetic reprogramming, metabolic disorders, inflammation, and oxidative stress in forming of “impaired phenotype” of MPs. The incorporation of measurement of the endothelial cell-derived MP number into a conventional CV risk factor model aimed improving of risk stratification of the dysmetabolic patients with high probability of CV disease is discussed.\",\"PeriodicalId\":15630,\"journal\":{\"name\":\"Journal of Data Mining in Genomics & Proteomics\",\"volume\":\"22 1\",\"pages\":\"1-3\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2016-04-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"35\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Data Mining in Genomics & Proteomics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4172/2153-0602.1000195\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Data Mining in Genomics & Proteomics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4172/2153-0602.1000195","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 35

摘要

2型糖尿病(T2DM)仍然是全球心血管(CV)死亡的主要原因。虽然肥胖和代谢综合征被认为是导致T2DM高风险的关键因素,但代谢异常状态进展的确切分子机制仍不完全清楚。有大量证据表明,内皮功能障碍是增加心血管风险的关键因素,代谢异常患者的血管损伤可能通过不同微颗粒(MP)群体之间的不平衡来调节。这篇简短的评论讨论了内皮细胞中凋亡MPs和活化MPs之间的比例受损的作用,这被认为是内皮细胞来源MPs的“受损表型”。它考虑了表观遗传重编程、代谢紊乱、炎症和氧化应激在MPs“受损表型”形成中的因果关系。本文讨论了将内皮细胞来源的MP数测量纳入传统的心血管危险因素模型,旨在改善高概率心血管疾病代谢异常患者的风险分层。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Impaired Immune Phenotype of Endothelial Cell-derived Micro Particles: The Missing Link between Diabetes-related States and Risk of Cardiovascular Complications?
Type two diabetes mellitus (T2DM) remains a leading contributor to cardiovascular (CV) mortality worldwide. Although obese and metabolic syndrome are discussed key factors contributing a higher risk of T2DM, the exact molecular mechanisms underlying to the progression of dysmetabolic states are still not completely clear. There is large body of evidence regarding endothelial dysfunction as a key player in increasing CV risk and that vascular damage in the dysmetabolic patients might mediate through an imbalance between various populations of micro particle (MP). The short commentary is discussed a role of impaired ratio between apoptotic MPs and activated MPs derived from endothelial cells that was recognized as “impaired phenotype” of endothelial cell-derived MPs. It has considered the causality epigenetic reprogramming, metabolic disorders, inflammation, and oxidative stress in forming of “impaired phenotype” of MPs. The incorporation of measurement of the endothelial cell-derived MP number into a conventional CV risk factor model aimed improving of risk stratification of the dysmetabolic patients with high probability of CV disease is discussed.
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:481959085
Book学术官方微信