Arterial Remodeling After Coronary Angioplasty

Mintz, Gary S.; Popma, Jeffrey J.; Pichard, Augusto D.; Kent, Kenneth M.; Satler, Lowell F.; Wong, S. Chiu; Hong, Mun K.; Kovach, Julie A.; Leon, Martin B.

doi:10.1161/01.cir.94.1.35

Cited by 776 publications

(181 citation statements)

References 81 publications

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“…2 accumulation plays a crucial role in the pathogenesis of vascular diseases, which include postangioplasty restenosis (1,2), and many studies aimed at explaining the molecular pathways regulating the myointimal hyperplastic process. Restenosis remains the most feared complication following percutaneous transluminal angioplasty (3).…”

Section: Intimal Smooth Muscle Cell (Smc)mentioning

confidence: 99%

“…In vivo, daily PLC treatment 15 days after injury resulted in a reduction of relative rat aortic intimal volume, an increase of apoptosis, Bax up-regulation without changing the Bcl-2 level, and a reduction of NF-B, vascular cell adhesion molecule-1, monocyte chemotactic protein-1, and survivin in myointimal thickening compared with controls. In the presence of 10% serum, a reduced G 1 …”

mentioning

confidence: 99%

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Propionyl-L-carnitine Reduces Proliferation and Potentiates Bax-related Apoptosis of Aortic Intimal Smooth Muscle Cells by Modulating Nuclear Factor-κB Activity

Orlandi

Francesconi

Marcellini

et al. 2007

Journal of Biological Chemistry

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Section: Intimal Smooth Muscle Cell (Smc)mentioning

confidence: 99%

mentioning

confidence: 99%

Propionyl-L-carnitine Reduces Proliferation and Potentiates Bax-related Apoptosis of Aortic Intimal Smooth Muscle Cells by Modulating Nuclear Factor-κB Activity

Orlandi

Francesconi

Marcellini

et al. 2007

Journal of Biological Chemistry

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“…Three principle mechanisms of restenosis after balloon angioplasty have been identified: elastic recoil, negative remodelling and neointimal hyperplasia (2)(3)(4). Coronary stenting prevents acute elastic recoil and negative remodelling, but does not have any effect against neointimal formation (5).…”

Section: Mechanisms Of Restenosismentioning

confidence: 99%

The cell cycle: A critical therapeutic target to prevent vascular proliferative disease

Charron

Nili

Strauss

2006

Canadian Journal of Cardiology

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“…6 -8 In humans, vascular remodeling but not intimal lesion formation was shown to account for the majority of the restenosis in response to angioplasty procedures. 9,10 We have recently established and characterized a mouse model of arterial remodeling. 11 In this model, flow in the common carotid artery is interrupted by ligation of the vessel near the carotid bifurcation.…”

mentioning

confidence: 99%

Strain-Dependent Vascular Remodeling Phenotypes in Inbred Mice

Harmon¹,

Couper²,

Lindner³

2000

The American Journal of Pathology

120

104

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Vascular remodeling is a response of blood vessels to both physiological and pathological stimuli, leading to either vessel enlargement (positive remodeling) or reduction in vessel diameter (negative remodeling). Examples of remodeling have been observed in fetal development 1 and after graft placement 2-5 or angioplasty. 6 -8 In humans, vascular remodeling but not intimal lesion formation was shown to account for the majority of the restenosis in response to angioplasty procedures. 9,10 We have recently established and characterized a mouse model of arterial remodeling. 11 In this model, flow in the common carotid artery is interrupted by ligation of the vessel near the carotid bifurcation. Using FVB/NJ mice, this resulted in a dramatic reduction in vessel diameter and formation of an intimal lesion. Neointima formation and the influx of inflammatory cells in this model are reduced in P-selectin-deficient mice, while the reduction in vessel diameter is not affected by the lack of P-selectin. 12 Additional specific factors that mediate the remodeling response are beginning to emerge. Several studies have implicated nitric oxide (NO) as an inhibitor of remodeling events. [13][14][15][16][17] Our own studies demonstrated that alterations in blood flow also lead to changes in gene expression of platelet-derived growth factor Achain and B-chain, factors known to modulate proliferation and migration of smooth muscle cells (SMC). 18 Preliminary experiments in our laboratory indicated that there is wide qualitative and quantitative variation in the vascular remodeling response of different mouse strains. To provide the basis for a genetic analysis, we subjected 11 different strains of inbred mice to carotid artery ligation for analysis of the remodeling response. Large differences were found between strains with regards to negative as well as positive remodeling and intimal lesion formation. The magnitude of neointima formation correlated with increased loss of SMC occurring immediately after ligation of the carotid artery as well as enhanced growth properties of SMC in vitro.

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Arterial Remodeling After Coronary Angioplasty

Abstract: Restenosis appears to be determined primarily by the direction and magnitude of vessel wall remodeling (delta EEM). An increase in EEM is adaptive, whereas a decrease in EEM contributes to restenosis.

Cited by 776 publications

References 81 publications

Propionyl-L-carnitine Reduces Proliferation and Potentiates Bax-related Apoptosis of Aortic Intimal Smooth Muscle Cells by Modulating Nuclear Factor-κB Activity

Propionyl-L-carnitine Reduces Proliferation and Potentiates Bax-related Apoptosis of Aortic Intimal Smooth Muscle Cells by Modulating Nuclear Factor-κB Activity

The cell cycle: A critical therapeutic target to prevent vascular proliferative disease

Strain-Dependent Vascular Remodeling Phenotypes in Inbred Mice

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