Hypoxia But Not Inflammation Augments Glucose Uptake in Human Macrophages

Folco, Eduardo J.; Sheikine, Yuri; Rocha, Viviane Z.; Christen, Thomas; Shvartz, Eugenia; Sukhova, Galina K.; Carli, Marcelo F. Di; Libby, Peter

doi:10.1016/j.jacc.2011.03.044

Cited by 293 publications

(155 citation statements)

References 55 publications

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“…Hypoxia and HIF1α expression has been shown in vitro to alter macrophage lipid handling and suppress cholesterol efflux via ABCA1 (the ATP-binding cassette subfamily A member 1) in both mouse 127 and human 128 macrophages. Moreover, in vitro and ex vivo experiments have implicated hypoxia and HIF1α in driving enhanced glucose uptake, metabolic activity, and polarization of macrophages in human atheroma 129 .…”

Section: Atherosclerosis Pathogenesismentioning

confidence: 99%

Erratum: Inflammatory processes in cardiovascular disease: a route to targeted therapies

Ruparelia¹,

Chai²,

Fisher³

et al. 2017

Nat Rev Cardiol

192

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Inflammatory processes are firmly established as central to the development and complications of cardiovascular diseases. Elevated levels of inflammatory markers have been shown to be predictive of future cardiovascular events. The specific targeting of these processes in experimental models has been shown to attenuate myocardial and arterial injury, reduce disease progression, and promote healing. However, the translation of these observations and the demonstration of clear efficacy in clinical practice have been disappointing. A major limitation might be that tools currently used to measure 'inflammation' are insufficiently precise and do not provide information about disease site, activity, or discriminate between functionally important activation pathways. The challenge, therefore, is to make measures of inflammation that are more meaningful, and which can guide specific targeted therapies. In this Review, we consider the roles of inflammatory processes in the related pathologies of atherosclerosis and acute myocardial infarction (AMI), by providing an evaluation of the known and emerging inflammatory pathways. We highlight contemporary techniques to characterize and quantify inflammation, and consider how they might be used to guide specific treatments. Finally, we discuss emerging opportunities in the field, including current limitations and challenges that are the focus of ongoing study.Inflammation and its failure to resolve are firmly established as central to the development and complications of several cardiovascular diseases [1][2][3] . Elevated levels of markers of inflammation, such as C-reactive protein (CRP) and serum amyloid A (SAA), have been shown to be predictive of future cardiovascular events across a range of clinical settings [4][5][6] . The role of the innate immune system in the pathogenesis of cardiovascular diseases has been an area of particular focus, with the appreciation that targeting innate immune function Correspondence to R.P.C.: robin.choudhury@cardiov.ox.ac.uk. Author contributionsAll the authors researched data for the article, discussed its contents, and wrote, reviewed, and edited the manuscript before submission. Competing interests statementThe authors declare no competing interests. HHS Public AccessAuthor manuscript Nat Rev Cardiol. Author manuscript; available in PMC 2017 September 01. Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript in experimental models can variously attenuate disease progression and injury, and promote healing [7][8][9][10] .Processes of inflammation contribute to a broad range of cardiovascular diseases; however, in this Review, we consider the roles of inflammatory processes in the related pathologies of atherosclerosis and acute myocardial infarction (AMI), by providing an evaluation of known and emerging inflammatory pathways that are thought to be central to their pathogenesis, and the consequences of their activation. We highlight contemporary techniques to characterize and quantify inflammation, and consider h...

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Section: Atherosclerosis Pathogenesismentioning

confidence: 99%

Erratum: Inflammatory processes in cardiovascular disease: a route to targeted therapies

Ruparelia¹,

Chai²,

Fisher³

et al. 2017

Nat Rev Cardiol

192

View full text Add to dashboard Cite

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“…First, as most metabolically active cells take up glucose, it is unclear how much of the observed signal is influenced by cells other than macrophages within plaques, including neutrophils, lymphocytes, endothelial cells, and vascular smooth muscle cells. Vascular 18 F-FDG signal intensity is also significantly influenced by plaque hypoxia and therefore might not be purely representative of inflammation per se [125]. Perhaps most importantly, using 18 F-FDG to image the coronary vasculature is particularly difficult because of high background myocardial uptake of 18 F-FDG, even with strict dietary manipulation or prolonged fasting [126].…”

Section: Positron Emission Tomographymentioning

confidence: 99%

Invasive or non-invasive imaging for detecting high-risk coronary lesions?

Patel

Tarkin

Serruys

et al. 2017

Expert Review of Cardiovascular Therapy

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Introduction: Advances in our understanding about atherosclerotic evolution have enabled us to identify specific plaque characteristics that are associated with coronary plaque vulnerability and cardiovascular events. With constant improvements in signal and image processing an arsenal of invasive and non-invasive imaging modalities have been developed that are capable of identifying these features allowing in vivo assessment of plaque vulnerability. Areas covered: This review article presents the available and emerging imaging modalities introduced to assess plaque morphology and biology, describes the evidence from the first large scale studies that evaluated the efficacy of invasive and non-invasive imaging in detecting lesions that are likely to progress and cause cardiovascular events and discusses the potential implications of the in vivo assessment of coronary artery pathology in the clinical setting. Expert commentary: Invasive imaging, with its high resolution, and in particular hybrid intravascular imaging appears as the ideal approach to study the mechanisms regulating atherosclerotic disease progression; whereas non-invasive imaging is expected to enable complete assessment of coronary tree pathology, detection of high-risk lesions, more accurate risk stratification and thus to allow a personalized treatment of vulnerable patients. ARTICLE HISTORY

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“…In addition to the coronary circulation, other limitations to 18 F-FDG imaging in atherosclerosis include spillover from residual blood pool activity into the arterial walls, dependence of uptake on blood glucose levels that can be problematic in diabetics, and experimental data showing that hypoxia stimulates 18 F-FDG uptake in macrophages while proinflammatory cytokines stimulate uptake of 18 F-FDG in endothelial cells and smooth muscle cells. 8,10 For these reasons, the search for alternative tracers targeting vascular inflammation is currently an area of active interest.…”

Section: See Related Article Pp 862-871mentioning

confidence: 99%

Targeting activated macrophages to identify the vulnerable atherosclerotic plaque

Johnson

2017

Journal of Nuclear Cardiology

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Hypoxia But Not Inflammation Augments Glucose Uptake in Human Macrophages

Abstract: Glucose uptake and, probably, FdG uptake signals in atheroma may reflect hypoxia-stimulated macrophages rather than mere inflammatory burden. Cytokine-activated smooth-muscle cells also may contribute to the FdG signal.

Cited by 293 publications

References 55 publications

Erratum: Inflammatory processes in cardiovascular disease: a route to targeted therapies

Erratum: Inflammatory processes in cardiovascular disease: a route to targeted therapies

Invasive or non-invasive imaging for detecting high-risk coronary lesions?

Targeting activated macrophages to identify the vulnerable atherosclerotic plaque

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