Hypoxia and Inflammation
| Autor: | Ian Wilcox, Jo-Dee L. Lattimore, Kim H. Chan |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Procollagen-Proline Dioxygenase
Inflammation Adaptive Immunity Infections Article Proinflammatory cytokine Immunity Neoplasms Basic Helix-Loop-Helix Transcription Factors medicine Animals Humans Hypoxia Transcription factor Sleep Apnea Obstructive Toll-like receptor business.industry Inflammatory Bowel Diseases Inflammasome General Medicine Hypoxia (medical) Atherosclerosis Acquired immune system medicine.disease Immunity Innate Review article Immunology Hypoxia-Inducible Factor 1 medicine.symptom business Reperfusion injury Homeostasis Signal Transduction medicine.drug |
| Zdroj: | New England Journal of Medicine. 364:1976-1977 |
| ISSN: | 1533-4406 0028-4793 |
| Popis: | 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 leads to secretion of proinflammatory cytokines, in particular interleukin-1β,2 resulting in neutrophilic inflammation. The NLRP3 inflammasome mechanism was first discovered in autosomal autoinflammatory syndromes, namely cryopyrin-associated periodic syndromes, and these disorders have responded beautifully to interleukin-1–targeted therapies. Now there is current interest among several pharmaceutical companies to test similar therapies in inflammatory disorders caused by hypoxic–ischemic reperfusion injury.2-4 |
| Databáze: | OpenAIRE |
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