Restenosis following coronary balloon angioplasty

Liu, Ming Wei; Berk, Bradford C.

doi:10.1016/1050-1738(91)90003-w

Cited by 16 publications

(3 citation statements)

References 19 publications

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“…Macrophage‐derived growth factor, cytokines from neutrophils and lymphocytes, and other inflammatory mediators are mitogenic and/or chemotactic for VSMC [130]. Growth factors are the primary mediators of proliferation and migration of VSMC and have been reviewed by Berk [131].…”

Section: Factors Involved In Restenosismentioning

confidence: 99%

Do Statins have a Role in Reduction/Prevention of Post‐PCI Restenosis?

Prasad

2011

Cardiovascular Therapeutics

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SUMMARYThe pathophysiology of post-PCI restenosis involves neointimal formation that consists of three phases: thrombosis (within 24 h), recruitment (3-8 days), and proliferation, which starts on day 8 of PCI. Various factors suggested to be predictors/risks for restenosis include C-reactive protein (CRP), inflammatory mediators (cytokines and adhesion molecules), oxygen radicals, advanced glycation end products (AGEs) and their receptors (RAGE), and soluble RAGE (sRAGE). The earlier noted factors produce thrombogenesis, vascular smooth muscle cell proliferation, and extracellular matrix formation. Statins have pleiotropic effects. Besides lowering serum cholesterol, they have various other biological effects including antiinflammatory, antithrombotic, CRP-lowering, antioxidant, antimitotic, and inhibition of smooth muscle cell proliferation. They inhibit matrix metalloproteinase and cyclooxygenase-2, lower AGEs, decrease expression of RAGE and increase levels of serum sRAGE. They also increase the synthesis of nitric oxide (NO) by increasing endothelial NO synthase expression and activity. Preprocedural statin therapy is known to reduce peri-and post-PCI myonecrosis and reduce the need for repeat revascularization. There is evidence that statin-eluting stents inhibit in-stent restenosis in animal models. It is concluded that because of the above attributes of statins, they are suitable candidates for reduction of post-PCI restenosis and post-PCI myonecrosis. The future directions for the use of statins in reduction of post-PCI restenosis and myonecrosis have been discussed.

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Section: Factors Involved In Restenosismentioning

confidence: 99%

Do Statins have a Role in Reduction/Prevention of Post‐PCI Restenosis?

Prasad

2011

Cardiovascular Therapeutics

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“…An accelerated form of this proliferative process appears to play a central role in the restenosis that occurs after angioplasty 1 and in premature artery disease in transplanted organs. 2 Release of growth-promoting factors by endothelial cells, macrophages, and activated platelets at the site of vascular injury leads to migration and proliferation of SMCs that may ultimately contribute to the intimal thickening observed in vascular stenosis.…”

Section: S Mooth Muscle Cell (Smc) Proliferation Accountsmentioning

confidence: 99%

Polymorphonuclear leukocytes enhance release of growth factors by cultured endothelial cells.

Totani¹,

Piccoli²,

Pellegrini³

et al. 1994

Arterioscler Thromb

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Porcine aortic endothelial cells (PAECs) in culture constitutivery secrete polypeptide (endothelium-derived) growth factors (EDGFs) into the surrounding medium. Incubation of PAECs with human peripheral blood polymorphonuclear leukocytes (PMNs) caused a significant increase in EDGF release as assessed by pH]thymidine incorporation into BALB/c 3T3 mouse fibroblasts and cell proliferation assay. The effect was time dependent and correlated with the number of PMNs, reaching a maximum with a 1:1 PAEC to PMN ratio. Generation of mitogenic activity was prevented by cycloheximide, indicating a requirement for de novo protein synthesis. Antibody-mediated inhibition assays suggested that mitogenic activity was due to platelet-derived growth factor and basic fibroblast growth factor. When supernatant from N-formyl-methionyl-leucyl-phenylalanine-stimulated PMNs was substituted for PMNs during incubation with PAECs, powerful mitogenic activity was generated, indicating the involvement of soluble mediators. A role for free oxygen radicals was ruled out by experiments in which superoxide dismutase and catalase did not prevent the increase in mitogenic activity. By contrast, serine protease inhibitors such as soybean trypsin inhibitor, a^antitrypsin, and eglin C reduced the PMN-stimulating activity by 70%, 80%, and 100%, respectively. The possible involvement of cathepsin G and elastase was investigated. Cathepsin G and elastase, when substituted for PMNs, increased the release of EDGFs in a dose-dependent fashion, mimicking the effect of PMNs. These findings suggest a new role for leukocyte-vessel wall interactions in the proliferative feature of atherosclerosis. (Arterioscler Thromb. 1994;14:125-132.)

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“…The aberrant proliferation of vascular smooth muscles cells (VSMCs) has been reputed to play a critical role in atherosclerosis and restenosis . Accordingly, 6c was evaluated in an 8 day RAVSMC growth delay assay to assess the ability of this compound to inhibit VSMC proliferation in cell culture (Figure )…”

mentioning

confidence: 99%

Structure−Activity Relationships for a Novel Series of Pyrido[2,3-d]pyrimidine Tyrosine Kinase Inhibitors

Hamby¹,

Connolly²,

Schroeder³

et al. 1997

J. Med. Chem.

131

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Screening of a compound library for inhibitors of the fibroblast growth factor (FGFr) and platelet-derived growth factor (PDGFr) receptor tyrosine kinases led to the development of a novel series of ATP competitive pyrido[2,3-d]pyrimidine tyrosine kinase inhibitors. The initial lead, 1-[2-amino-6-(2,6-dichlorophenyl)pyrido[2,3-d]pyrimidin-7-yl]-3- tert-butylurea (4b, PD-089828), was found to be a broadly active tyrosine kinase inhibitor. Compound 4b inhibited the PDGFr, FGFr, EGFr, and c-src tyrosine kinases with IC50 values of 1.11, 0.13, 0.45, and 0.22 microM, respectively. Subsequent SAR studies led to the synthesis of new analogs with improved potency, solubility, and bioavailability relative to the initial lead. For example, the introduction of a [4-(diethylamino)butyl]amino side chain into the 2-position of 4b afforded compound 6c with enhanced potency and bioavailability. Compound 6c inhibited PDGF-stimulated vascular smooth muscle cell proliferation with an IC50 of 0.3 microM. Furthermore, replacement of the 6-(2,6-dichlorophenyl) moiety of 4b with a 6-(3',5'-dimethoxyphenyl) functionality produced a highly selective FGFr tyrosine kinase inhibitor 4e. Compound 4e inhibited the FGFr tyrosine kinase with an IC50 of 0.060 microM, whereas IC50s for the inhibition of the PDGFr, FGFr, EGFr, c-src, and InsR tyrosine kinases for this compound (4e) were all greater than 50 microM.

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Restenosis following coronary balloon angioplasty

Cited by 16 publications

References 19 publications

Do Statins have a Role in Reduction/Prevention of Post‐PCI Restenosis?

Do Statins have a Role in Reduction/Prevention of Post‐PCI Restenosis?

Polymorphonuclear leukocytes enhance release of growth factors by cultured endothelial cells.

Structure−Activity Relationships for a Novel Series of Pyrido[2,3-d]pyrimidine Tyrosine Kinase Inhibitors

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