• 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

Evidence that the death of macrophage foam cells contributes to the lipid core of atheroma.

作者信息

Ball R Y, Stowers E C, Burton J H, Cary N R, Skepper J N, Mitchinson M J

机构信息

Department of Histopathology, Norfolk and Norwich Health Care NHS Trust, UK.

出版信息

Atherosclerosis. 1995 Apr 7;114(1):45-54. doi: 10.1016/0021-9150(94)05463-s.

DOI:10.1016/0021-9150(94)05463-s
PMID:7605375
Abstract

Sections of human atherosclerotic lesions of different stages show that, in early lesions, the acellular lipid core is usually immediately adjacent to the deepest edge of a collection of macrophage foam cells. Advanced lesions with a large lipid core have variable numbers of macrophage foam cells, close to the lateral edges, or shoulders, of the core. In both early and advanced lesions, some of the macrophages nearest the core appear to be dying. Lipid cores contain two materials which in earlier lesions are found only in macrophages, namely ceroid and CD68 antigen, but do not contain recognisable smooth muscle cell actin. It is concluded that death of macrophage foam cells contributes to the origin and slow enlargement of the lipid core. The cause of macrophage death is not yet certain, but is under investigation.

摘要

相似文献

1
Evidence that the death of macrophage foam cells contributes to the lipid core of atheroma.
Atherosclerosis. 1995 Apr 7;114(1):45-54. doi: 10.1016/0021-9150(94)05463-s.
2
Foam cell apoptosis and the development of the lipid core of human atherosclerosis.泡沫细胞凋亡与人类动脉粥样硬化脂质核心的形成
J Pathol. 1996 Dec;180(4):423-9. doi: 10.1002/(SICI)1096-9896(199612)180:4<423::AID-PATH677>3.0.CO;2-1.
3
Apoptotic macrophage-derived foam cells of human atheromas are rich in iron and ferritin, suggesting iron-catalysed reactions to be involved in apoptosis.人类动脉粥样硬化斑块中凋亡的巨噬细胞源性泡沫细胞富含铁和铁蛋白,这表明铁催化反应参与了细胞凋亡。
Free Radic Res. 1999 Mar;30(3):221-31. doi: 10.1080/10715769900300241.
4
A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association.动脉粥样硬化病变的高级类型定义及动脉粥样硬化的组织学分类。美国心脏协会动脉硬化理事会血管病变委员会的报告。
Circulation. 1995 Sep 1;92(5):1355-74. doi: 10.1161/01.cir.92.5.1355.
5
Phenotype determination of anti-GM3 positive cells in atherosclerotic lesions of the human aorta. Hypothetical role of ganglioside GM3 in foam cell formation.人主动脉动脉粥样硬化病变中抗GM3阳性细胞的表型测定。神经节苷脂GM3在泡沫细胞形成中的假设作用。
Biochim Biophys Acta. 2001 Feb 14;1535(2):87-99. doi: 10.1016/s0925-4439(00)00076-4.
6
Human aortic fibrolipid lesions. Progenitor lesions for fibrous plaques, exhibiting early formation of the cholesterol-rich core.人类主动脉纤维脂质病变。纤维斑块的祖细胞病变,表现出富含胆固醇核心的早期形成。
Am J Pathol. 1985 Aug;120(2):193-206.
7
Foam cells and atherogenesis.泡沫细胞与动脉粥样硬化形成
Ann N Y Acad Sci. 1985;454:79-90. doi: 10.1111/j.1749-6632.1985.tb11846.x.
8
[Immunocytochemical investigations of cardiac and vessel allograft arteriosclerosis using smooth muscle cell and macrophage-specific monoclonal antibodies].[使用平滑肌细胞和巨噬细胞特异性单克隆抗体对心脏和血管同种异体移植动脉硬化进行免疫细胞化学研究]
Nihon Geka Gakkai Zasshi. 1989 Nov;90(11):1840-7.
9
Macrophage foam cells and atherosclerosis.巨噬细胞泡沫细胞与动脉粥样硬化。
Front Biosci. 2001 Mar 1;6:D429-55. doi: 10.2741/kruth.
10
Identification of foam cells in human atherosclerotic lesions as macrophages using monoclonal antibodies.利用单克隆抗体将人类动脉粥样硬化病变中的泡沫细胞鉴定为巨噬细胞。
Arch Pathol Lab Med. 1985 May;109(5):445-9.

引用本文的文献

1
Apolipoprotein A1 deficiency increases macrophage apoptosis and necrotic core development in atherosclerotic plaques in a Bim-dependent manner.载脂蛋白A1缺乏以Bim依赖的方式增加动脉粥样硬化斑块中巨噬细胞凋亡和坏死核心的形成。
J Lipid Res. 2025 May;66(5):100782. doi: 10.1016/j.jlr.2025.100782. Epub 2025 Mar 20.
2
Drug screen identifies verteporfin as a regulator of lipid metabolism in macrophage foam cells.药物筛选鉴定维替泊芬是泡沫细胞中巨噬细胞脂代谢的调节剂。
Sci Rep. 2023 Nov 9;13(1):19588. doi: 10.1038/s41598-023-46467-4.
3
Haemodynamic Effects on the Development and Stability of Atherosclerotic Plaques in Arterial Blood Vessel.
血流动力学对动脉血管中动脉粥样硬化斑块发展及稳定性的影响
Interdiscip Sci. 2023 Dec;15(4):616-632. doi: 10.1007/s12539-023-00576-w. Epub 2023 Jul 7.
4
Membrane Cholesterol Interactions with Proteins in Hypercholesterolemia-Induced Endothelial Dysfunction.胆固醇通过与膜蛋白相互作用在高胆固醇血症诱导的血管内皮功能障碍中的作用
Curr Atheroscler Rep. 2023 Sep;25(9):535-541. doi: 10.1007/s11883-023-01127-w. Epub 2023 Jul 7.
5
Loss of Macrophage mTORC2 Drives Atherosclerosis via FoxO1 and IL-1β Signaling.巨噬细胞 mTORC2 的缺失通过 FoxO1 和 IL-1β 信号通路驱动动脉粥样硬化。
Circ Res. 2023 Jul 21;133(3):200-219. doi: 10.1161/CIRCRESAHA.122.321542. Epub 2023 Jun 23.
6
miR-126 promotes M1 to M2 macrophage phenotype switching VEGFA and KLF4.miR-126 促进 M1 到 M2 巨噬细胞表型转换 VEGF 和 KLF4。
PeerJ. 2023 Mar 31;11:e15180. doi: 10.7717/peerj.15180. eCollection 2023.
7
The emerging role of pyroptosis-related inflammasome pathway in atherosclerosis.焦亡相关炎性小体通路在动脉粥样硬化中的新兴作用。
Mol Med. 2022 Dec 21;28(1):160. doi: 10.1186/s10020-022-00594-2.
8
Case Report: Next Generation Sequencing in Clinical Practice-A Real Tool for Ending the Protracted Diagnostic Odyssey.病例报告:临床实践中的下一代测序——结束漫长诊断之旅的实用工具。
Front Cardiovasc Med. 2022 Jan 13;8:778961. doi: 10.3389/fcvm.2021.778961. eCollection 2021.
9
K-80003 Inhibition of Macrophage Apoptosis and Necrotic Core Development in Atherosclerotic Vulnerable Plaques.K-80003 抑制动脉粥样硬化易损斑块中的巨噬细胞凋亡和坏死核心形成。
Cardiovasc Drugs Ther. 2022 Dec;36(6):1061-1073. doi: 10.1007/s10557-021-07237-4. Epub 2021 Aug 19.
10
STAT5 inhibitor attenuates atherosclerosis via inhibition of inflammation: the role of STAT5 in atherosclerosis.信号转导和转录激活因子5(STAT5)抑制剂通过抑制炎症减轻动脉粥样硬化:STAT5在动脉粥样硬化中的作用
Am J Transl Res. 2021 Mar 15;13(3):1422-1431. eCollection 2021.