2013
DOI: 10.1007/s40256-013-0017-4
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Inhibition of Atherosclerosis by Angiotensin II Type 1 Receptor Antagonists

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Cited by 7 publications
(9 citation statements)
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“…responses and oxidative stress of various cell types such as endothelium, VSMCs, and macrophages, within atherosclerotic plaques (27,28). AngII upregulates the expression of various pro-inflammatory mediators in VSMCs including TNF-α, MCP-1, IL-6 and nitric oxide synthase (29).…”
Section: Discussionmentioning
confidence: 99%
“…responses and oxidative stress of various cell types such as endothelium, VSMCs, and macrophages, within atherosclerotic plaques (27,28). AngII upregulates the expression of various pro-inflammatory mediators in VSMCs including TNF-α, MCP-1, IL-6 and nitric oxide synthase (29).…”
Section: Discussionmentioning
confidence: 99%
“…Neointima was composed of various characteristic lesions, such as fibrous tissue, proteoglycan-rich tissue, approved by pathologic examination of restenosis in bare-metal stent (BMS) and in DES in tissue samples obtained by atherectomy [ 20 ]. In the other hand, ARBs inhibit atherosclerosis as reduced plaque burden in atherosclerotic vessels and reduced incidence of in-stent restenosis [ 21 ]. In this concept of anti-inflammatory and anti-proliferative effect of ARBs toward atherosclerosis and neointimal growth, our present study assessed difference of neointimal characterization in use of long term ARBs by OCT.…”
Section: Discussionmentioning
confidence: 99%
“…Available data suggest that the beneficial effects of ARBs on atherosclerosis cannot be considered a class effect. Losartan and candesartan have not shown any effect on atherosclerosis or on in-stent restenosis, but valsartan, olmesartan and telmisartan appear to have a significant beneficial effect [ 21 ]. Also, various types of DES were used, from first generation (SES) to second generation (EES, BES, ZES), limiting this study that second-generation DES lead to a lower percentage of uncovered and malapposed struts, as well as a lower incidence of intra-stent thrombi, compared with first-generation DES [ 28 , 29 ].…”
Section: Discussionmentioning
confidence: 99%
“…However, the level of NO did not change ( in animal models of atherosclerosis [19]. In atheromatous plaque 157 area where macrophages and foam cells, also, accumulate, high 158 concentrations of tissue ACE will produce large amounts of Ang II.…”
Section: Genementioning
confidence: 97%
“…The incidence of coronary heart disease is 17 usually low, where the population of plasma cholesterol levels are 18 low [1]. 19 Atherosclerosis is considered a chronic and progressive disease 20 that may be induced by the injury of the arterial endothelium, 21 proliferation of vascular smooth muscle cells (VSMC), and 22 accumulation of lipids in vessel walls. It is often associated with 23 hypertension, elevated low-density lipoprotein (LDL) and de-24 creased high-density lipoprotein (HDL) levels, and diabetes 25 mellitus [2,3].…”
Section: Q2mentioning
confidence: 99%