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Hypoxia in Plaque Macrophages A New Danger Signal for Interleukin-1&bgr; Activation?

Hypoxia in Plaque Macrophages A New Danger Signal for Interleukin-1&bgr; Activation? Editorial Hypoxia in Plaque Macrophages A New Danger Signal for Interleukin-1β Activation? Ismail Sergin, Trent D. Evans, Somashubhra Bhattacharya, Babak Razani he recruitment of inflammatory cells to the arterial aberrant lipid metabolism in the atherosclerotic plaque, have Twall and their critical role in increasing plaque size and now been shown to be potent inducers of the NLRP3 inflam- complexity is now dogma in the field of atherosclerosis. masome and IL-1β secretion in macrophages, akin to other 4–6 Macrophages compose the majority of the inflammatory bur - crystalline damage-associated molecular patterns. Even the den in plaques and incite many of the deleterious responses proinflammatory action of oxidized low-density lipoprotein that exacerbate disease. Thus, the mechanisms by which mac- seems to occur in part through CD36-mediated uptake into rophages are activated to secrete cytokines and other inflam- lysosomes and conversion to cholesterol crystals. matory mediators are of intense interest. The atherosclerotic Given the ability of IL-1β to further enhance the proinflam- milieu is replete with cellular stressors such as modified apo- matory response and recruitment of immune cells, its critical lipoprotein B–containing lipoproteins (eg, oxidized low-den- role in exacerbating atherosclerotic progression has long been sity lipoprotein) and reactive oxygen species, which http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Circulation Research Wolters Kluwer Health

Hypoxia in Plaque Macrophages A New Danger Signal for Interleukin-1&bgr; Activation?

Razani, Babak
Circulation Research , Volume 115 (10) – Oct 1, 2014
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References (31)

Copyright
© 2014 American Heart Association, Inc.
ISSN
0009-7330
eISSN
1524-4571
DOI
10.1161/CIRCRESAHA.114.305197
pmid
25342768
Publisher site
See Article on Publisher Site

Abstract

Editorial Hypoxia in Plaque Macrophages A New Danger Signal for Interleukin-1β Activation? Ismail Sergin, Trent D. Evans, Somashubhra Bhattacharya, Babak Razani he recruitment of inflammatory cells to the arterial aberrant lipid metabolism in the atherosclerotic plaque, have Twall and their critical role in increasing plaque size and now been shown to be potent inducers of the NLRP3 inflam- complexity is now dogma in the field of atherosclerosis. masome and IL-1β secretion in macrophages, akin to other 4–6 Macrophages compose the majority of the inflammatory bur - crystalline damage-associated molecular patterns. Even the den in plaques and incite many of the deleterious responses proinflammatory action of oxidized low-density lipoprotein that exacerbate disease. Thus, the mechanisms by which mac- seems to occur in part through CD36-mediated uptake into rophages are activated to secrete cytokines and other inflam- lysosomes and conversion to cholesterol crystals. matory mediators are of intense interest. The atherosclerotic Given the ability of IL-1β to further enhance the proinflam- milieu is replete with cellular stressors such as modified apo- matory response and recruitment of immune cells, its critical lipoprotein B–containing lipoproteins (eg, oxidized low-den- role in exacerbating atherosclerotic progression has long been sity lipoprotein) and reactive oxygen species, which

Journal

Circulation Research – Wolters Kluwer Health

Published: Oct 1, 2014

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