To the Editor: In their review article on hypoxia and inflammation, Eltzschig and Carmeliet (Feb. 17 issue)(1) were thorough in promoting the role of hypoxia-inducible transcription factor (HIF) and related mechanisms to regain homeostasis in hypoxic tissue environments. Although very exacting in its discussion, the review unfortunately failed to include other, equally important mechanisms that lead to inflammation from hypoxic-ischemic reperfusion injury. I am referring in part to the importance of the inflammasome, and in particular to the NLRP3 inflammasome that responds to danger-associated molecular patterns (e.g., urates, free ATP) resulting from nucleoprotein catabolism induced by such injury. Such stimulation . . .
CITATION STYLE
Eltzschig, H. K., & Carmeliet, P. (2011). Hypoxia and Inflammation. New England Journal of Medicine, 364(7), 656–665. https://doi.org/10.1056/nejmra0910283
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