• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

重新审视胆固醇逆转运:胆汁与肠道胆固醇排泄的贡献。

Reverse cholesterol transport revisited: contribution of biliary versus intestinal cholesterol excretion.

机构信息

Department of Pediatrics, University Medical Center Groningen, University of Groningen, The Netherlands.

出版信息

Arterioscler Thromb Vasc Biol. 2011 Aug;31(8):1726-33. doi: 10.1161/ATVBAHA.108.181206. Epub 2011 May 12.

DOI:10.1161/ATVBAHA.108.181206
PMID:21571685
Abstract

Reverse cholesterol transport (RCT) is usually defined as high-density lipoprotein-mediated transport of excess cholesterol from peripheral tissues, including cholesterol-laden macrophages in vessel walls, to the liver. From the liver, cholesterol can then be removed from the body via secretion into the bile for eventual disposal via the feces. According to this paradigm, high plasma high-density lipoprotein levels accelerate RCT and hence are atheroprotective. New insights in individual steps of the RCT pathway, in part derived from innovative mouse models, indicate that the classical concept of RCT may require modification.

摘要

胆固醇逆向转运(RCT)通常被定义为高密度脂蛋白介导的外周组织中胆固醇的转运,包括血管壁中载脂巨噬细胞的胆固醇,至肝脏。从肝脏中,胆固醇可以通过分泌到胆汁中,最终通过粪便排出体外。根据这一模式,高血浆高密度脂蛋白水平加速了 RCT,因此具有抗动脉粥样硬化作用。RCT 途径中各个步骤的新见解,部分源自创新的小鼠模型,表明 RCT 的经典概念可能需要修正。

相似文献

1
Reverse cholesterol transport revisited: contribution of biliary versus intestinal cholesterol excretion.重新审视胆固醇逆转运:胆汁与肠道胆固醇排泄的贡献。
Arterioscler Thromb Vasc Biol. 2011 Aug;31(8):1726-33. doi: 10.1161/ATVBAHA.108.181206. Epub 2011 May 12.
2
CD36-mediated cholesterol efflux is associated with PPARgamma activation via a MAPK-dependent COX-2 pathway in macrophages.在巨噬细胞中,CD36介导的胆固醇外流通过依赖丝裂原活化蛋白激酶(MAPK)的环氧合酶-2(COX-2)途径与过氧化物酶体增殖物激活受体γ(PPARγ)激活相关。
Cardiovasc Res. 2009 Aug 1;83(3):457-64. doi: 10.1093/cvr/cvp118. Epub 2009 Apr 17.
3
EP 80317, a CD36 selective ligand, promotes reverse cholesterol transport in apolipoprotein E-deficient mice.EP 80317,一种 CD36 选择性配体,可促进载脂蛋白 E 缺陷小鼠的胆固醇逆转运。
Atherosclerosis. 2013 Aug;229(2):408-14. doi: 10.1016/j.atherosclerosis.2013.05.031. Epub 2013 Jun 14.
4
Coffee consumption enhances high-density lipoprotein-mediated cholesterol efflux in macrophages.喝咖啡可增强巨噬细胞中高密度脂蛋白介导的胆固醇外流。
Circ Res. 2010 Mar 5;106(4):779-87. doi: 10.1161/CIRCRESAHA.109.206615. Epub 2010 Jan 14.
5
Hepatobiliary cholesterol transport is not impaired in Abca1-null mice lacking HDL.在缺乏高密度脂蛋白(HDL)的Abca1基因敲除小鼠中,肝胆胆固醇转运并未受损。
J Clin Invest. 2001 Sep;108(6):843-50. doi: 10.1172/JCI12473.
6
Reverse cholesterol transport and future pharmacological approaches to the treatment of atherosclerosis.逆向胆固醇转运与动脉粥样硬化治疗的未来药理学方法
Curr Opin Investig Drugs. 2001 Mar;2(3):375-81.
7
New insights into the regulation of HDL metabolism and reverse cholesterol transport.高密度脂蛋白代谢与胆固醇逆向转运调控的新见解。
Circ Res. 2005 Jun 24;96(12):1221-32. doi: 10.1161/01.RES.0000170946.56981.5c.
8
Rate-limiting factors of cholesterol efflux in reverse cholesterol transport: acceptors and donors.胆固醇逆转运中胆固醇流出的限速因素:接受体和供体。
Clin Exp Pharmacol Physiol. 2010 Jul;37(7):703-9. doi: 10.1111/j.1440-1681.2010.05386.x. Epub 2010 Mar 30.
9
In vivo macrophage-specific RCT and antioxidant and antiinflammatory HDL activity measurements: New tools for predicting HDL atheroprotection.体内巨噬细胞特异性逆向胆固醇转运以及抗氧化和抗炎高密度脂蛋白活性测量:预测高密度脂蛋白抗动脉粥样硬化保护作用的新工具。
Atherosclerosis. 2009 Oct;206(2):321-7. doi: 10.1016/j.atherosclerosis.2008.12.044. Epub 2009 Mar 21.
10
Reverse cholesterol transport and cholesterol efflux in atherosclerosis.动脉粥样硬化中的胆固醇逆向转运与胆固醇流出
QJM. 2005 Dec;98(12):845-56. doi: 10.1093/qjmed/hci136. Epub 2005 Oct 28.

引用本文的文献

1
Role of Protein Regulators of Cholesterol Homeostasis in Immune Modulation and Cancer Pathophysiology.胆固醇稳态的蛋白质调节因子在免疫调节和癌症病理生理学中的作用
Endocrinology. 2025 Feb 27;166(4). doi: 10.1210/endocr/bqaf031.
2
Gut Microbiota and Metabolic Syndrome: Relationships and Opportunities for New Therapeutic Strategies.肠道微生物群与代谢综合征:关系及新治疗策略的机遇
Scientifica (Cairo). 2024 Jul 15;2024:4222083. doi: 10.1155/2024/4222083. eCollection 2024.
3
Silicon as a Functional Meat Ingredient Improves Jejunal and Hepatic Cholesterol Homeostasis in a Late-Stage Type 2 Diabetes Mellitus Rat Model.
硅作为一种功能性肉类成分可改善晚期2型糖尿病大鼠模型的空肠和肝脏胆固醇稳态。
Foods. 2024 Jun 7;13(12):1794. doi: 10.3390/foods13121794.
4
Dietary Lysophosphatidylcholine Improves the Uptake of Astaxanthin and Modulates Cholesterol Transport in Pacific White Shrimp .日粮溶血磷脂酰胆碱可提高太平洋白对虾虾青素的摄取并调节胆固醇转运
Antioxidants (Basel). 2024 Apr 23;13(5):505. doi: 10.3390/antiox13050505.
5
Self-Assembled nanoparticles Combining Berberine and Sodium Taurocholate for Enhanced Anti-Hyperuricemia Effect.自组装纳米粒子结合小檗碱和牛磺胆酸钠增强抗高尿酸血症作用。
Int J Nanomedicine. 2023 Jul 26;18:4101-4120. doi: 10.2147/IJN.S409513. eCollection 2023.
6
Dietary Cholesterol Supplementation Inhibits the Steroid Biosynthesis but Does Not Affect the Cholesterol Transport in Two Marine Teleosts: A Hepatic Transcriptome Study.膳食胆固醇补充抑制两种海洋硬骨鱼的类固醇生物合成但不影响胆固醇转运:一项肝脏转录组研究
Aquac Nutr. 2023 Jun 5;2023:2308669. doi: 10.1155/2023/2308669. eCollection 2023.
7
Increased TG to HDL-C ratio is associated with severity of drug-induced liver injury.甘油三酯与高密度脂蛋白胆固醇比值升高与药物性肝损伤的严重程度相关。
Sci Rep. 2023 Apr 27;13(1):6897. doi: 10.1038/s41598-023-34137-4.
8
The role of the gut microbiota in health and cardiovascular diseases.肠道微生物群在健康和心血管疾病中的作用。
Mol Biomed. 2022 Oct 11;3(1):30. doi: 10.1186/s43556-022-00091-2.
9
Transintestinal cholesterol excretion in health and disease.在健康和疾病中的肠内胆固醇排泄。
Curr Atheroscler Rep. 2022 Mar;24(3):153-160. doi: 10.1007/s11883-022-00995-y. Epub 2022 Feb 9.
10
High density lipoproteins mediate in vivo protection against staphylococcal phenol-soluble modulins.高密度脂蛋白介导体内对葡萄球菌酚溶性调节素的保护作用。
Sci Rep. 2021 Jul 28;11(1):15357. doi: 10.1038/s41598-021-94651-1.