Exploring the nature of atheroma and cardiovascular inflammation<i>in vivo</i>using positron emission tomography (PET)

Buscombe, J. R.

doi:10.1259/bjr.20140648

Cited by 16 publications

(10 citation statements)

References 31 publications

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“…Atherosclerosis is characterized by a spotty pattern corresponding to areas of macrophage infiltration (79,81,82) that are the histological hallmark of plaque inflammation (83,84). Inflammation plays a crucial role in the progression of atherosclerotic cdt.amegroups.com S13 Cardiovascular Diagnosis and Therapy, Vol 8, Suppl 1 April 2018 disease (60,83,85).…”

mentioning

confidence: 99%

Noninvasive aortic imaging

Baliyan¹,

Verdini²,

Meyersohn³

2018

Cardiovasc. Diagn. Ther.

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confidence: 99%

Noninvasive aortic imaging

Baliyan¹,

Verdini²,

Meyersohn³

2018

Cardiovasc. Diagn. Ther.

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“…The partial pressure of oxygen varies within the normal artery wall, even in health,24 and areas of profound hypoxia (<1% O 2 ) may prevail in regions of diseased artery, for example, in macrophage-rich regions of atheroma 25. Furthermore, 5% O 2 is not true hypoxia and is, in fact, a normal oxygen concentration for many tissues.…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin and a nonerythropoietic peptide analog promote aortic endothelial cell repair under hypoxic conditions: role of nitric oxide

Heikal¹,

Ghezzi²,

Mengozzi³

et al. 2016

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The cytoprotective effects of erythropoietin (EPO) and an EPO-related nonerythropoietic analog, pyroglutamate helix B surface peptide (pHBSP), were investigated in an in vitro model of bovine aortic endothelial cell injury under normoxic (21% O2) and hypoxic (1% O2) conditions. The potential molecular mechanisms of these effects were also explored. Using a model of endothelial injury (the scratch assay), we found that, under hypoxic conditions, EPO and pHBSP enhanced scratch closure by promoting cell migration and proliferation, but did not show any effect under normoxic conditions. Furthermore, EPO protected bovine aortic endothelial cells from staurosporine-induced apoptosis under hypoxic conditions. The priming effect of hypoxia was associated with stabilization of hypoxia inducible factor-1α, EPO receptor upregulation, and decreased Ser-1177 phosphorylation of endothelial nitric oxide synthase (NOS); the effect of hypoxia on the latter was rescued by EPO. Hypoxia was associated with a reduction in nitric oxide (NO) production as assessed by its oxidation products, nitrite and nitrate, consistent with the oxygen requirement for endogenous production of NO by endothelial NOS. However, while EPO did not affect NO formation in normoxia, it markedly increased NO production, in a manner sensitive to NOS inhibition, under hypoxic conditions. These data are consistent with the notion that the tissue-protective actions of EPO-related cytokines in pathophysiological settings associated with poor oxygenation are mediated by NO. These findings may be particularly relevant to atherogenesis and postangioplasty restenosis.

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“…In vasculitis, a linear, smooth vascular FGD uptake extending over long vessel segments is typically observed [2]. In contrast, atherosclerosis is characterized by an irregular, more limited, Bspotty^pattern [2], which corresponds to vascular areas more heavily infiltrated by macrophages, i.e., to unstable atheroma, which is potentially thrombogenic [3]. Consistent with this concept, PET has been demonstrated to be able to predict adverse cardiovascular events [4].…”

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confidence: 84%