 |
 | Home | Contact Us | FAQ | Search & Site Map | Link to Us |
 | Sign In | Join | Other 45 Sites in Network |
Medical Forum / General / Alternative / July 2008Iron In Arterial Plaque
Iron in arterial plaque: A modifiable risk factor for atherosclerosis. Sullivan JL Biochim Biophys Acta 2008 Jun 19. It has been proposed that iron depletion protects against cardiovascular disease. There is increasing evidence that one mechanism for this protection may involve a reduction in iron levels within atherosclerotic plaque. Large increases in iron concentration are seen in human atherosclerotic lesions in comparison to levels in healthy arterial tissue. In animal models, depletion of lesion iron levels in vivo by phlebotomy, systemic iron chelation treatment or dietary iron restriction reduces lesion size and/or increases plaque stability. A number of factors associated with increased arterial disease or increased cardiovascular events is also associated with increased plaque iron. In rats, infusion of angiotensin II increases ferritin levels and arterial thickness which are reversed by treatment with the iron chelator deferoxamine. In humans, a polymorphism for haptoglobin associated with increased cardiovascular disease is also characterized by increased lesional iron. Heme oxygenase 1 (HO1) is an important component of the system for mobilization of iron from macrophages. Human HO1 promoter polymorphisms causing weaker upregulation of the enzyme are associated with increased cardiovascular disease and increased serum ferritin. Increased cardiovascular disease associated with inflammation may be in part caused by elevated hepcidin levels that promote retention of iron within plaque macrophages. Defective retention of iron within arterial macrophages in genetic hemochromatosis may explain why there is little evidence of increased atherosclerosis in this disorder despite systemic iron overload. The reviewed findings support the concept that arterial plaque iron is a modifiable risk factor for atherogenesis. Biochimica et biophysica acta [Biochim Biophys Acta] Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk On Jul 18, 7:33 am, "ironjust...@aol.com" <ironjust...@aol.com> wrote:Iron in arterial plaque << ORIGINAL RESEARCH ARTICLE Overexpression of Transferrin Receptor and Ferritin Related to Clinical Symptoms and Destabilization of Human Carotid Plaques Wei Li*,1, Li-Hua Xu,1,2, Claes Forssell, Jerome L. Sullivan and Xi- Ming Yuan,3 * Division of Pharmacology; Division of Experimental Pathology, Department of Clinical and Experimental Medicine; Division of Vascular Surgery, Department of Medicine and Health Sciences, Faculty of Health Sciences, Linköping University, Linköping, SE-58185 Sweden; and Burnett College of Biomedical Sciences, University of Central Florida, Orlando, Florida 32816 To whom requests for reprints should be addressed at 3 Division of Experimental Pathology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. E-mail: yuan.ximing@inr.liu.se; yuanximing@gmail.com Accumulation of tissue iron has been implicated in development of atherosclerotic lesions mainly because of increased iron-catalyzed oxidative injury. However, it remains unknown whether cellular iron import and storage in human atheroma are related to human atheroma development. We found that transferrin receptor 1 (TfR1), a major iron importer, is highly expressed in foamy macrophages and some smooth muscle cells in intimal lesions of human carotid atheroma, mainly in cytoplasmic accumulation patterns. In 52 human carotid atherosclerotic lesions, TfR1 expression was positively correlated with macrophage infiltration, ectopic lysosomal cathepsin L, and ferritin expression. Highly expressed TfR1 and ferritin in CD68-positive macrophages were significantly associated with development and severity of human carotid plaques, smoking, and patient’s symptoms. The findings suggest that pathologic macrophage iron metabolism may contribute to vulnerability of human atheroma, established risk factors, and their clinical symptoms. The cytoplasmic overexpression of TfR1 may be the result of lysosomal dysfunction and ectopic accumulation of lysosomal cathepsin L caused by atheroma-relevant lipids in atherogenesis. Key Words: atherosclerosis • apoptosis • iron metabolism • lysosomes • macrophages • plaque rupture First published online April 29, 2008 Experimental Biology and Medicine 233:818-826 (2008) doi: 10.3181/0711-RM-320 © 2008 by the Society for Experimental Biology and Medicine Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > Iron in arterial plaque: A modifiable risk factor for atherosclerosis. > Sullivan JL [quoted text clipped - 37 lines] > > DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk |
Reply to this Message |
 Sign In
 Join
 My Latest Posts My Monitored Threads My Blog My Photo Gallery My Profile My Homepage Start New Thread Enable EMail Alerts Rate this Thread
|
©2009 Advenet LLC Privacy Policy - Terms of Use
This website includes both content owned or controlled by Advenet as well as content owned or controlled by third parties.