Down-regulation of miR-23b induces phenotypic switching of vascular smooth muscle cellsin vitroandin vivo
نویسندگان
چکیده
منابع مشابه
miR-663 and the miRaculous vascular smooth muscle phenotypic switch.
C ardiovascular diseases, such as ischemic heart disease and stroke, represent the number one cause of death worldwide. 1 In most cases, atherosclerosis and hypertension constitute the underlying causes for cardiovascular disease because it leads to arterial occlusion and impaired cardiac function, respectively. Therapeutic compensation of atherosclerotic artery occlusion by bypass grafting, an...
متن کاملOxidized phospholipids induce phenotypic switching of vascular smooth muscle cells in vivo and in vitro.
Atherosclerosis is a vascular disease characterized by lipid deposition and inflammation within the arterial wall. Oxidized phospholipids (oxPLs), such as 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (oxPAPC) and its constituents 1-palmytoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) and 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine (PGPC) are concentrated within a...
متن کاملPhenotypic Modulation of Vascular Smooth Muscle Cells:
G protein-coupled receptors regulate two major functions of vascular smooth muscle cells (SMCs) the vasomotor contractile response and the proliferative response. The contractile phenotype of SMCs has mainly been studied in situ within intact blood vessels, whereas the synthetic or proliferative SMC phenotypes can be studied in culture and represent a model of the SMC phenotype seen in vascular...
متن کاملVascular smooth muscle phenotypic diversity and function.
The control of force production in vascular smooth muscle is critical to the normal regulation of blood flow and pressure, and altered regulation is common to diseases such as hypertension, heart failure, and ischemia. A great deal has been learned about imbalances in vasoconstrictor and vasodilator signals, e.g., angiotensin, endothelin, norepinephrine, and nitric oxide, that regulate vascular...
متن کاملSmooth Muscle–Selective Inhibition of Nuclear Factor‐κB Attenuates Smooth Muscle Phenotypic Switching and Neointima Formation Following Vascular Injury
BACKGROUND Vascular proliferative diseases such as atherosclerosis are inflammatory disorders involving multiple cell types including macrophages, lymphocytes, endothelial cells, and smooth muscle cells (SMCs). Although activation of the nuclear factor-κB (NF-κB) pathway in vessels has been shown to be critical for the progression of vascular diseases, the cell-autonomous role of NF-κB within S...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Cardiovascular Research
سال: 2015
ISSN: 0008-6363,1755-3245
DOI: 10.1093/cvr/cvv141