Triglyceride-Rich Lipoproteins: Their Role in Atherosclerosis.

Yulino Castillo-Núñez, Enrique Morales-Villegas, Carlos A Aguilar-Salinas
{"title":"Triglyceride-Rich Lipoproteins: Their Role in Atherosclerosis.","authors":"Yulino Castillo-Núñez,&nbsp;Enrique Morales-Villegas,&nbsp;Carlos A Aguilar-Salinas","doi":"10.24875/RIC.21000416","DOIUrl":null,"url":null,"abstract":"<p><p>The term \"triglyceride-rich lipoproteins\" (TRLs) includes chylomicrons and their remnants, very low-density lipoproteins (VLDL), and intermediate-density lipoproteins (IDL). In this manuscript, the mechanisms by which atherogenic TRLs contribute to the formation of atheroma plaques are reviewed. Cholesterol from TRLs that can be retained in the subendothelial space (i.e., remnants, DLs, and small VLDLs) contributes to the genesis of atherosclerosis. Triglycerides of atherogenic TRLs induce inflammation of the arterial wall. Mechanisms that explain the involvement of TRLs in atherosclerosis are the generation of pro-atherogenic changes in high-density lipoproteins and low-density lipoproteins, accumulation of TRLs in plasma, and their passage to the subendothelial space where they cause endothelial dysfunction and inflammation of the vascular wall. Furthermore, plasma accumulation of TRLs causes hyperviscosity and a procoagulant state. Finally, this manuscript summarizes the controversial aspects of the clinical approach and the treatment of cases with dyslipidemia explained by atherogenic TRLs.</p>","PeriodicalId":49612,"journal":{"name":"Revista De Investigacion Clinica-Clinical and Translational Investigation","volume":"74 2","pages":"061-070"},"PeriodicalIF":1.4000,"publicationDate":"2022-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"12","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Revista De Investigacion Clinica-Clinical and Translational Investigation","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.24875/RIC.21000416","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 12

Abstract

The term "triglyceride-rich lipoproteins" (TRLs) includes chylomicrons and their remnants, very low-density lipoproteins (VLDL), and intermediate-density lipoproteins (IDL). In this manuscript, the mechanisms by which atherogenic TRLs contribute to the formation of atheroma plaques are reviewed. Cholesterol from TRLs that can be retained in the subendothelial space (i.e., remnants, DLs, and small VLDLs) contributes to the genesis of atherosclerosis. Triglycerides of atherogenic TRLs induce inflammation of the arterial wall. Mechanisms that explain the involvement of TRLs in atherosclerosis are the generation of pro-atherogenic changes in high-density lipoproteins and low-density lipoproteins, accumulation of TRLs in plasma, and their passage to the subendothelial space where they cause endothelial dysfunction and inflammation of the vascular wall. Furthermore, plasma accumulation of TRLs causes hyperviscosity and a procoagulant state. Finally, this manuscript summarizes the controversial aspects of the clinical approach and the treatment of cases with dyslipidemia explained by atherogenic TRLs.

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
富甘油三酯脂蛋白:在动脉粥样硬化中的作用。
“富含甘油三酯的脂蛋白”(trl)包括乳糜微粒及其残余物、极低密度脂蛋白(VLDL)和中密度脂蛋白(IDL)。本文综述了致动脉粥样硬化trl促进动脉粥样硬化斑块形成的机制。来自trl的胆固醇可以保留在内皮下空间(即残留物,DLs和小vldl)有助于动脉粥样硬化的发生。致动脉粥样硬化trl的甘油三酯诱导动脉壁炎症。trl参与动脉粥样硬化的机制是高密度脂蛋白和低密度脂蛋白的促动脉粥样硬化改变的产生,trl在血浆中的积累,它们进入内皮下空间,在那里它们引起内皮功能障碍和血管壁炎症。此外,血浆中trl的积累导致高粘度和促凝状态。最后,本文总结了由动脉粥样硬化性trl引起的血脂异常的临床方法和治疗中有争议的方面。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
3.00
自引率
0.00%
发文量
60
审稿时长
>12 weeks
期刊介绍: The Revista de Investigación Clínica – Clinical and Translational Investigation (RIC-C&TI), publishes original clinical and biomedical research of interest to physicians in internal medicine, surgery, and any of their specialties. The Revista de Investigación Clínica – Clinical and Translational Investigation is the official journal of the National Institutes of Health of Mexico, which comprises a group of Institutes and High Specialty Hospitals belonging to the Ministery of Health. The journal is published both on-line and in printed version, appears bimonthly and publishes peer-reviewed original research articles as well as brief and in-depth reviews. All articles published are open access and can be immediately and permanently free for everyone to read and download. The journal accepts clinical and molecular research articles, short reports and reviews. Types of manuscripts: – Brief Communications – Research Letters – Original Articles – Brief Reviews – In-depth Reviews – Perspectives – Letters to the Editor
期刊最新文献
Proposal of a functional prognostic scale in mexican patients with Guillain-Barré syndrome. LINC01614 activated by SP1 promoted malignant behavior of triple-negative breast cancer cells via the WNT/b-Catenin signaling pathway. Expanding Diagnostic Workup for hypertensive Intracerebral hemorrhage: a retrospective LATAM cerebrovascular registry comparison. Genotypes distribution of the SNP RS1477196 of FTO gen associated with primary knee osteoarthritis in females: an analysis using the 100Genomes database. Validation of the HAS-BLED scale for the assessment of bleeding risk in patients on anticoagulation therapy with a diagnosis of venous thromboembolic 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