2004
DOI: 10.1016/j.clim.2004.03.021
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Modulation of tachykinin and cytokine release in patients with coronary disease undergoing percutaneous revascularization

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Cited by 14 publications
(10 citation statements)
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References 32 publications
(30 reference statements)
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“…The largest amount of data are available with regards to IL-1 and IL-6, both in animal models with ACS [34,35] and in humans [36][37][38], whereas evidences on TNF are contrasting: Pudil et al did not find any release of TNF in subjects with ACS [38], while other authors showed increased TNF levels during ACS [36,37,39]. In a paper by Fichtlscherer et al., enrolling patients with endothelial dysfunction, higher levels of IL-10 were demonstrated in subjects with a less compromised endothelial reserve [40], while lower concentrations were found in patients with ACS [21,41]. There are fewer data regarding IL-2, IL-18, and IFN [39], particularly during the first 24 h of ACS.…”
Section: Discussionmentioning
confidence: 89%
“…The largest amount of data are available with regards to IL-1 and IL-6, both in animal models with ACS [34,35] and in humans [36][37][38], whereas evidences on TNF are contrasting: Pudil et al did not find any release of TNF in subjects with ACS [38], while other authors showed increased TNF levels during ACS [36,37,39]. In a paper by Fichtlscherer et al., enrolling patients with endothelial dysfunction, higher levels of IL-10 were demonstrated in subjects with a less compromised endothelial reserve [40], while lower concentrations were found in patients with ACS [21,41]. There are fewer data regarding IL-2, IL-18, and IFN [39], particularly during the first 24 h of ACS.…”
Section: Discussionmentioning
confidence: 89%
“…Inflammatory mechanisms have been indicated to play a pivotal role in neointimal formation and restenosis. The pleiotropic pro-inflammatory cytokine IFN-γ has been implicated in the pathogenic processes of restenosis (11)(12)(13). However, IFN-γ has been shown to both promote (11) and inhibit (14) injury-mediated neointimal formation, and therefore warrants further investigation.…”
Section: A B Cmentioning
confidence: 99%
“…Activation of IFN-γ signalling in neointimal SMCs was indicated in 37 of the 223 differentially expressed genes in atherectomy specimens of patients with restenosis, determined by a transcriptome study (13). Furthermore, elevated circulating IFN-γ has been detected within 15 min following stent implantation, in both chronic and acute coronary syndrome patients undergoing angioplasty, suggesting that modulation of IFN-γ release plays a role in inflammatory complications of angioplasty during/following stenting (12). Animal studies concerning the role of IFN-γ on injury-mediated models of neointimal formation have yielded (11), and exogenous IFN-γ treatment (14) reduced injury-induced neointimal formation in rats.…”
Section: Introductionmentioning
confidence: 98%
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“…[5][6][7][8][9] Cytokines such as interferon gamma (IFN-γ) and tumour necrosis factor alpha (TNF-α) increase pro-inflammatory activity during and following PCI and might therefore be related to long-term complications after an intervention. 10 Patients with T2DM display increased plasma levels of inflammatory markers, and deteriorating glycaemic control is associated with particularly sensitive to this complication. This has not, however, been fully explored in controlled clinical trials.…”
Section: Introductionmentioning
confidence: 99%