{"title":"CVD中VSMC炎症的表观遗传猝灭:H3K9me2在控制中。","authors":"E. Lutgens","doi":"10.1161/ATVBAHA.119.313345","DOIUrl":null,"url":null,"abstract":"According to the old dogma of atherosclerotic plaque development, vascular smooth muscle cells (VSMCs) are the matrix-producing engines of the atherosclerotic plaque that grow the fibrous cap and are a responsible for maintaining plaque stability.1 Plaque VSMCs start of as contractile VSMCs in the media, where they, on injury, are recruited to the intima and undergo phenotypic conversion toward proliferative synthetic cells that produce and deposit extracellular matrix.1","PeriodicalId":8404,"journal":{"name":"Arteriosclerosis, Thrombosis, & Vascular Biology","volume":"19 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Epigenetic Quenching of VSMC Inflammation in CVD: H3K9me2 in Control.\",\"authors\":\"E. Lutgens\",\"doi\":\"10.1161/ATVBAHA.119.313345\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"According to the old dogma of atherosclerotic plaque development, vascular smooth muscle cells (VSMCs) are the matrix-producing engines of the atherosclerotic plaque that grow the fibrous cap and are a responsible for maintaining plaque stability.1 Plaque VSMCs start of as contractile VSMCs in the media, where they, on injury, are recruited to the intima and undergo phenotypic conversion toward proliferative synthetic cells that produce and deposit extracellular matrix.1\",\"PeriodicalId\":8404,\"journal\":{\"name\":\"Arteriosclerosis, Thrombosis, & Vascular Biology\",\"volume\":\"19 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-10-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Arteriosclerosis, Thrombosis, & Vascular Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1161/ATVBAHA.119.313345\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Arteriosclerosis, Thrombosis, & Vascular Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1161/ATVBAHA.119.313345","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Epigenetic Quenching of VSMC Inflammation in CVD: H3K9me2 in Control.
According to the old dogma of atherosclerotic plaque development, vascular smooth muscle cells (VSMCs) are the matrix-producing engines of the atherosclerotic plaque that grow the fibrous cap and are a responsible for maintaining plaque stability.1 Plaque VSMCs start of as contractile VSMCs in the media, where they, on injury, are recruited to the intima and undergo phenotypic conversion toward proliferative synthetic cells that produce and deposit extracellular matrix.1