878. Overexpression of Fibromodulin Inhibits Neointima Formation in Cultured Human Saphenous Veins

Ranjzad, Parisa; Salem, Husein K.; Kingston, Paul A.

doi:10.1016/j.ymthe.2006.08.966

Cited by 1 publication

(2 citation statements)

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“…Decorin has also been shown to result in a significant inhibition of neointimal hyperplasia, a precursor of advanced atherosclerosis in an ex vivo human saphenous vein graft model. Ranzad and colleagues provided direct evidence for this concept by overexpressing decorin via adenovirus transfection in the human saphenous vein segments in association with a marked reduction in neointimal hyperplasia [Ranjzad et al 2009]. This observation of reduction in neointimal hyperplasia with decorin overexpression strongly suggests that development of agents based on decorin structure may be of potential therapeutic value.…”

Section: Distribution Of Decorin In Normal and Atherosclerotic Arteriesmentioning

confidence: 99%

“…In fact, decorin may prove to be a starter given that related molecules of SLRP family, such as fibromodulin, have been shown to inhibit neo-intimal hyperplasia in saphenous venous grafts [Ranjzad et al 2009]. Conceptually, local delivery of decorin at the site of coronary stenting (analogous to delivery of antimitotic drugs to prevent in-stent restenosis) may prove to be useful at it will not only decrease the risk of restenosis, but also decrease the risk of in-stent thrombosis by promoting endothelial healing.…”

Section: Perspectivementioning

confidence: 99%

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Decorin in atherosclerosis

Singla¹,

Hu²,

Mizeracki³

et al. 2011

Therapeutic Advances in Cardiovascular Disease

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Atherosclerotic cardiovascular disease is a major cause of morbidity and mortality in the Western world. Despite tremendous strides in understandings its pathogenesis, it still remains a challenge because of gaps in our understanding of its initiation, progression and complications leading to the clinical syndromes of angina, acute coronary syndrome, cerebrovascular disease and peripheral vascular disease. Recent studies have provided impetus on the shift from models of atherosclerosis based on cellular interactions to models where the important role of extracellular matrix is recognized. Proteoglycans, especially those belonging to the small leucine-rich proteoglycan family of which decorin is a representative example, have come under close scrutiny for their role in atherogenesis. There is evidence from in vitro and in vivo animal models as well as humans to suggest an important role of decorin in attenuating progression of atherosclerosis. Decorin distribution in different blood vessels has been shown to inversely correlate with the tendency to develop atherosclerosis. Decorin seems to interact closely with different cellular components of the plaque milieu, thereby suggesting its role in influencing atherogenesis at different steps. Here we review the current understanding of the role of decorin in the pathogenesis of atherosclerosis.

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Section: Distribution Of Decorin In Normal and Atherosclerotic Arteriesmentioning

confidence: 99%

Section: Perspectivementioning

confidence: 99%