Cytokine therapy for arterial restenosis: inhibition of neointimal hyperplasia by gamma-interferon*1, *2

Castronuovo, John J.; Guss, Stephen B.; Mysh, D.; Sawhney, Aanchal; Wolff, Marianne; Gown, Allen M.

doi:10.1016/0967-2109(95)94442-y

Cited by 15 publications

(4 citation statements)

References 24 publications

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“…Wang et al (2007) demonstrated that increased expression of IFN--induced SMC proliferation and intimal expansion in mouse. In contrast, and Castronuovo et al (1995) demonstrated that injection of IFN- into rat decreased IH after balloon injury. All of these studies used a model overexpressing IFN- (by adenovirus or directly by injection of IFN-).…”

Section: Discussionmentioning

confidence: 94%

Targeting PI3Kγ activity decreases vascular trauma-induced intimal hyperplasia through modulation of the Th1 response

Smirnova

Gayral

Pedros

et al. 2014

Journal of Experimental Medicine

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Section: Discussionmentioning

confidence: 94%

Targeting PI3Kγ activity decreases vascular trauma-induced intimal hyperplasia through modulation of the Th1 response

Smirnova

Gayral

Pedros

et al. 2014

Journal of Experimental Medicine

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“…For instance, it was shown that the administration of IFN-γ inhibited intimal thickening after arterial injury [79,80]. Inhibition of TGF-β reduced collagen accumulation in atherosclerotic arteries from apo E deficient mice and accelerates atherosclerosis and induces an unstable plaque phenotype in mice [81,82].…”

Section: Interventional Studies Inhibiting Collagen Synthesismentioning

confidence: 99%

Modulation of Collagen Turnover in Cardiovascular Disease

Rodríguez-Feo¹,

Sluijter²,

Kleijn³

et al. 2005

CPD

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Collagen fibers are the most abundant components of the extracellular matrix in arteries and myocardium. Disturbances in the collagen turnover (synthesis and degradation) have been linked to inflammatory diseases including cardiovascular pathological syndromes. In the myocardium, changes in collagen turnover may result in ventricle dilatation and subsequent contractile dysfunction. In arteries, collagen synthesis and degradation are associated with the progression of atherosclerotic disease and intimal hyperplasia following injury. Collagen synthesis is tightly regulated at several levels: synthesis of procollagens, suitable folding of polypeptides, secretion and cross-linking of mature fibers. On the other hand, degradation of newly synthesised procollagen and mature collagen fibers depends on the action of Matrix-Metalloproteinases (MMPs). The major role of collagen turnover in cardiovascular disorders has stimulated the search for pharmacological agents that interfere with collagen turnover at different levels. These drugs can theoretically act through modulation of the synthesis of procollagens or by interference with their post-translational modifications. Another group of pharmacological agents inhibit collagen breakdown (MMP inhibitors). Beneficial effects of compounds that target collagen metabolism have been reported. Unfortunately, many of these compounds also give rise to serious adverse effects due to interference with vital biological processes in which collagen plays an important role. In this paper, we will review cardiovascular diseases in which altered local collagen turnover is a key feature. Subsequently, the effect of compounds that have been developed and tested to modulate collagen synthesis, cross-linking or breakdown will be discussed.

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“…Interferon-γ was demonstrated to inhibit SMC proliferation without endothelial cell toxicity in vitro [149,150]. Further animal studies are needed to confirm these encouraging results.…”

Section: Ongoing Preclinical and Clinical Research For The Preventionmentioning

confidence: 71%

The drug-based pipeline against restenosis

Keller

Ibrahim²,

Tardif³

2005

Expert Opinion on Emerging Drugs

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More than 1 million percutaneous coronary interventions (PCIs) are performed yearly worldwide. Restenosis is the recurrent narrowing that can occur within 6 months following an initially successful PCI. Although drug-eluting stents have accomplished remarkable success, restenosis has not been eliminated and optimisation of both the polymers and drugs associated with them is desirable. This article reviews the presently available and potential preventive approaches against restenosis, including the sirolimus and paclitaxel drug-eluting stents.

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Cytokine therapy for arterial restenosis: inhibition of neointimal hyperplasia by gamma-interferon1, 2

Cited by 15 publications

References 24 publications

Targeting PI3Kγ activity decreases vascular trauma-induced intimal hyperplasia through modulation of the Th1 response

Targeting PI3Kγ activity decreases vascular trauma-induced intimal hyperplasia through modulation of the Th1 response

Modulation of Collagen Turnover in Cardiovascular Disease

The drug-based pipeline against restenosis

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