نتایج جستجو برای: intimal pathology
تعداد نتایج: 114322 فیلتر نتایج به سال:
Where do intimal smooth muscle cells (SMCs) come from? For many years, the idea that intimal SMCs originated from the underlying media went unchallenged.1 Then, reports2,3 began to appear that up to half of the SMCs in the intima of atherosclerotic plaques and injured arteries arose from circulating progenitor cells of bone marrow origin. This new view of intimal SMC formation was potentially i...
Atherosclerosis is an inflammatory disease of the artery characterized by an expansion of the intimal region. Intimal thickening is usually attributed to the migration of smooth muscle cells (SMCs) from the surrounding media and proliferation of SMCs already present in the intima. Intimal expansion can give rise to dangerous events such as stenosis (leading to stroke) or plaque rupture (leading...
Cigarette smoke is associated with increased carotid intimal thickening or stroke. Preliminary work showed that exposure to smoke resulted in a 4.5-fold reduction of heat shock protein-70 (HSP70) expression in spleens of mice using gene microarray analysis. In the current study, we investigated the role of extracellular HSP70 in carotid intimal thickening of mice exposed to cigarette smoke. Int...
Reductions in nitric oxide (NO) activity persist after arterial intimal injury and may be a factor in the development of intimal hyperplasia. NO inhibits in vitro platelet aggregation, leukocyte adhesion, and smooth muscle cell growth, all of which are key components in the process of intimal hyperplasia. We hypothesized that long-term supplementation with L-arginine, the precursor of NO, would...
We studied the influence of hypophyseetomy on endothelial cell regrowth and intimal thickening following aortic endothelial removal. Modification of this influence by replacement doses of glucocorticoids, mineralocorticoids, thyroxin, and growth hormone also was investigated. Young adult male rats were used, and endothelial removal was achieved by the balloon catheter method. Percent endothelia...
OBJECTIVE Drug-eluting stent delivery of mTORC1 (mechanistic target of rapamycin complex 1) inhibitors is highly effective in preventing intimal hyperplasia after coronary revascularization, but adverse effects limit their use for systemic vascular disease. Understanding the mechanism of action may lead to new treatment strategies. We have shown that rapamycin promotes vascular smooth muscle ce...
BACKGROUND Intimal hyperplasia after stent implantation is the main cause of in-stent restenosis. Activated monocytes play a key role in intimal growth. The anti-inflammatory cytokine interleukin-10 (IL-10) is a potent monocyte deactivator, endogenously produced in the atherosclerotic plaque. We tested the hypothesis that exogenous IL-10 may limit postangioplasty intimal hyperplasia after ballo...
OBJECTIVE Genetic P300/CBP-associated factor (PCAF) variation affects restenosis-risk in patients. PCAF has lysine acetyltransferase activity and promotes nuclear factor kappa-beta (NFκB)-mediated inflammation, which drives post-interventional intimal hyperplasia development. We studied the contributing role of PCAF in post-interventional intimal hyperplasia. METHODS AND RESULTS PCAF contribu...
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