Trapidil (triazolopyrimidine), a platelet-derived growth factor antagonist, reduces restenosis after percutaneous transluminal coronary angioplasty. Results of the randomized, double-blind STARC study. Studio Trapidil versus Aspirin nella Restenosi Coronarica.

Maresta, A; Balducelli, Marco; Cantini, Luca; Casari, A; Chioin, R; Fabbri, Mauro; Fontanelli, A; Preti, P.; Repetto, S; Servi, Stefano De

doi:10.1161/01.cir.90.6.2710

Cited by 134 publications

(52 citation statements)

References 13 publications

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“…The present findings of very low plasma insulin and serum platelet-derived growth factor levels in the CR group provide preliminary evidence that CR also results in a decreased stimulus for cell proliferation in humans. Platelet-derived growth factor is a potent chemoattractant and mitogen for vascular smooth muscle cells, and some drugs that counteract its biological actions have been developed for the treatment of atherosclerosis (43,44).…”

Section: Discussionmentioning

confidence: 99%

Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans

Fontana

Meyer

Klein

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

803

625

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Little is known regarding the long-term effects of caloric restriction (CR) on the risk for atherosclerosis. We evaluated the effect of CR on risk factors for atherosclerosis in individuals who are restricting food intake to slow aging. We studied 18 individuals who had been on CR for an average of 6 years and 18 age-matched healthy individuals on typical American diets. We measured serum lipids and lipoproteins, fasting plasma glucose and insulin, blood pressure (BP), high-sensitivity C-reactive protein (CRP), platelet-derived growth factor AB (PDGF-AB), body composition, and carotid artery intima-media thickness (IMT). The CR group were leaner than the comparison group (body mass index, 19.6 ؎ 1.9 vs. 25.9 ؎ 3.2 kg͞m 2 ; percent body fat, 8.7 ؎ 7% vs. 24 ؎ 8%). Serum total cholesterol (Tchol), low-density lipoprotein cholesterol, ratio of Tchol to high-density lipoprotein cholesterol (HDL-C), triglycerides, fasting glucose, fasting insulin, CRP, PDFG-AB, and systolic and diastolic BP were all markedly lower, whereas HDL-C was higher, in the CR than in the American diet group. Medical records indicated that the CR group had serum lipid-lipoprotein and BP levels in the usual range for individuals on typical American diets, and similar to those of the comparison group, before they began CR. Carotid artery IMT was Ϸ40% less in the CR group than in the comparison group. Based on a range of risk factors, it appears that long-term CR has a powerful protective effect against atherosclerosis. This interpretation is supported by the finding of a low carotid artery IMT.

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Section: Discussionmentioning

confidence: 99%

Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans

Fontana

Meyer

Klein

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

803

625

View full text Add to dashboard Cite

show abstract

“…Several types of drug therapy, such as anticoagulants (heparin, warfarin) and antiplatelet therapy (aspirin, dipyridamole, ticlopidine, prostacyclin, and thromboxane A2 inhibitor), fish oil, and steroids have failed to reduce the restenosis rate in most clinical trials. [22][23][24] Recently, trapidil and cholesterol-lowering agents have been shown to be promising in preventing restenosis after coronary angioplasty, 25 but patients must take these drugs for several months after angioplasty.…”

Section: Previous and Present Trials Regarding The Prevention Of Restmentioning

confidence: 99%

Local Delivery of Argatroban for the Prevention of Restenosis After Coronary Balloon Angioplasty

Itoh

Nonogi

Miyazaki

et al. 2004

Circ J

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“…2 Furthermore, the PDGF antagonist trapidil (triazolopyrimidine) has been shown to reduce restenosis in both animals and humans. 3,4 Trapidil is an antiplatelet drug as well as a coronary vasodilator that exerts its action by inhibiting thromboxane A 2 and stimulating the synthesis and release of prostacyclin. 5,6 Moreover, trapidil has been shown to antagonize PDGF action.…”

mentioning

confidence: 99%

“…Because the effect of trapidil in vivo has been demonstrated after subacute to chronic administration, blockade at the receptor level seems unlikely to be the mechanism. 3,4 Cellular signaling for PDGF requires ligand activation of receptor, intrinsic receptor tyrosine kinase activation, and autophosphorylation of receptor. Autophosphorylation on multiple tyrosine residues increases the ability to bind and phosphorylate other proteins such as PLC␥, Ras GAP, PI3K, and an adaptor molecule Shc.…”

mentioning

confidence: 99%

Trapidil Inhibits Platelet-Derived Growth Factor–Stimulated Mitogen-Activated Protein Kinase Cascade

Hoshiya

Awazu

1998

Hypertension

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Abstract-Trapidil, an antiplatelet drug, has been shown to reduce restenosis after angioplasty. It exerts its action, at least in part, by inhibiting vascular smooth muscle cell proliferation, antagonizing platelet-derived growth factor (PDGF). We examined its site of action on PDGF cellular signaling. Exposure of cultured rat vascular smooth muscle cells to increasing concentrations of trapidil for 18 hours resulted in a dose-dependent reduction in PDGF-BB-stimulated [ 3 H] thymidine incorporation. Trapidil (400 g/mL) increased PDGF ␤-receptor protein by 28Ϯ8%, whereas PDGF-induced tyrosine phosphorylation of PDGF ␤-receptor remained unchanged. PDGF-induced tyrosine phosphorylation of phospholipase C␥, the p85 regulatory subunit of phosphatidyl-inositol 3 kinase, Ras GTPase-activating protein, and an adaptor molecule Shc were also not altered. On the other hand, trapidil inhibited PDGF-stimulated mitogen-activated protein kinase (MAP kinase) activity by 35Ϯ7% at 10 minutes and by 32Ϯ10% at 6 hours. Activation of Raf-1, an upstream activator of MAP kinase, by PDGF was also attenuated by trapidil. Moreover, protein content of MAP kinase phosphatase-1, which inactivates MAP kinase, was elevated in trapidil-treated cells. These actions of trapidil may be mediated by cAMP. Thus, there was a 1.9-fold increase in cellular cAMP generation in trapidil-treated cells. The present results demonstrate that trapidil antagonizes PDGF-induced mitogenesis and MAP kinase activation in vascular smooth muscle cells, probably through cAMP. (Hypertension. 1998;31:665-671.)

show abstract

Trapidil (triazolopyrimidine), a platelet-derived growth factor antagonist, reduces restenosis after percutaneous transluminal coronary angioplasty. Results of the randomized, double-blind STARC study. Studio Trapidil versus Aspirin nella Restenosi Coronarica.

Abstract: Trapidil reduces restenosis after PTCA at the dosage of 100 mg TID and favorably influences the clinical outcome thereafter.

Cited by 134 publications

References 13 publications

Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans

Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans

Local Delivery of Argatroban for the Prevention of Restenosis After Coronary Balloon Angioplasty

Trapidil Inhibits Platelet-Derived Growth Factor–Stimulated Mitogen-Activated Protein Kinase Cascade

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