平滑肌细胞和基质金属蛋白酶作为动脉粥样硬化斑块稳定靶点的表型调节

G. Chaldakov, M. Zhelyazkova-Savova, Daniela Panayotova, M. Fiore, S. Yanev
{"title":"平滑肌细胞和基质金属蛋白酶作为动脉粥样硬化斑块稳定靶点的表型调节","authors":"G. Chaldakov, M. Zhelyazkova-Savova, Daniela Panayotova, M. Fiore, S. Yanev","doi":"10.14748/BMR.V31.7704","DOIUrl":null,"url":null,"abstract":"Atherosclerosis and its complications, erosion and rupture of the plaque fibrous cap, lead to myocardial infarction and stroke, the main causes of mortality worldwide. In this setting, arterial smooth muscle cells (SMC) of the innermost media undergo phenotypic changes, a switch towards a secretory phenotype engaged in matrix proteins production. In its nature, this is a protective action that forms of a new arterial layer, the fibrous cap covering the plaque thrombogenic lipid core. The risk of plaque rupture is inversely correlated with the presence of secretory state SMC and collagen fibrils within the fibrous cap. Thus, fibrous cap remodeling appears to be the main determinant of plaque vulnerability. Herein, we focus on the potential role of (i) the transcription factors TCF21 and KLF-4 in SMC phenotypic modulation, (ii) the matrix protein secretion of SMC, and (iii) the activity of proteinases (MMP, ADAM, ADAMTS, furin, and the MMP inducer CD147) in this critical process. We argue that focusing on these basic pathways could contribute to the knowledge of fibrous cap stability that might be translated into clinical medicine.","PeriodicalId":8906,"journal":{"name":"Biomedical Reviews","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2020-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Phenotypic modulation of smooth muscle cells and matrix metalloproteinases as targets for atherosclerotic plaque stabilization\",\"authors\":\"G. Chaldakov, M. Zhelyazkova-Savova, Daniela Panayotova, M. Fiore, S. Yanev\",\"doi\":\"10.14748/BMR.V31.7704\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Atherosclerosis and its complications, erosion and rupture of the plaque fibrous cap, lead to myocardial infarction and stroke, the main causes of mortality worldwide. In this setting, arterial smooth muscle cells (SMC) of the innermost media undergo phenotypic changes, a switch towards a secretory phenotype engaged in matrix proteins production. In its nature, this is a protective action that forms of a new arterial layer, the fibrous cap covering the plaque thrombogenic lipid core. The risk of plaque rupture is inversely correlated with the presence of secretory state SMC and collagen fibrils within the fibrous cap. Thus, fibrous cap remodeling appears to be the main determinant of plaque vulnerability. Herein, we focus on the potential role of (i) the transcription factors TCF21 and KLF-4 in SMC phenotypic modulation, (ii) the matrix protein secretion of SMC, and (iii) the activity of proteinases (MMP, ADAM, ADAMTS, furin, and the MMP inducer CD147) in this critical process. We argue that focusing on these basic pathways could contribute to the knowledge of fibrous cap stability that might be translated into clinical medicine.\",\"PeriodicalId\":8906,\"journal\":{\"name\":\"Biomedical Reviews\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-05-07\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biomedical Reviews\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.14748/BMR.V31.7704\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedical Reviews","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14748/BMR.V31.7704","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

动脉粥样硬化及其并发症,斑块纤维帽的侵蚀和破裂,可导致心肌梗死和中风,这是全世界死亡的主要原因。在这种情况下,最内层介质的动脉平滑肌细胞(SMC)发生表型改变,转向分泌型表型,参与基质蛋白的产生。从本质上讲,这是一种保护作用,形成新的动脉层,即覆盖斑块血栓形成的脂质核心的纤维帽。斑块破裂的风险与纤维帽内分泌状态SMC和胶原原纤维的存在呈负相关。因此,纤维帽重塑似乎是斑块易感性的主要决定因素。在此,我们重点研究了(i)转录因子TCF21和KLF-4在SMC表型调节中的潜在作用,(ii) SMC基质蛋白分泌,以及(iii)蛋白酶(MMP, ADAM, ADAMTS, furin和MMP诱导剂CD147)在这一关键过程中的活性。我们认为,关注这些基本途径可能有助于了解纤维帽稳定性,这可能会转化为临床医学。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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
Phenotypic modulation of smooth muscle cells and matrix metalloproteinases as targets for atherosclerotic plaque stabilization
Atherosclerosis and its complications, erosion and rupture of the plaque fibrous cap, lead to myocardial infarction and stroke, the main causes of mortality worldwide. In this setting, arterial smooth muscle cells (SMC) of the innermost media undergo phenotypic changes, a switch towards a secretory phenotype engaged in matrix proteins production. In its nature, this is a protective action that forms of a new arterial layer, the fibrous cap covering the plaque thrombogenic lipid core. The risk of plaque rupture is inversely correlated with the presence of secretory state SMC and collagen fibrils within the fibrous cap. Thus, fibrous cap remodeling appears to be the main determinant of plaque vulnerability. Herein, we focus on the potential role of (i) the transcription factors TCF21 and KLF-4 in SMC phenotypic modulation, (ii) the matrix protein secretion of SMC, and (iii) the activity of proteinases (MMP, ADAM, ADAMTS, furin, and the MMP inducer CD147) in this critical process. We argue that focusing on these basic pathways could contribute to the knowledge of fibrous cap stability that might be translated into clinical medicine.
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
期刊最新文献
Role of NANOG in glioma malignancy development and potential as therapeutic target A sample copy of the textbook Principles of Cell and Tissue Biology In defense of the murburn explanation for aerobic respiration The great Geoffrey Burnstock: A passion for discovery and empathy On the new prospects in biology inspired by epigenetics
×
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