Bench-to-bedside review: the effects of hyperoxia during critical illness

Abstract

During oxidative stress, mitochondrial damage is a pivotal cause of extracellular hazardous content including both free radicals and DAMPs. Because they resemble bacterial DNA, circulating mitochondrial DAMPs are efficiently recognized by pattern recognition receptors and activate polymorphonuclear neutrophils (PMNs). [...]oxidant scavenging can shift the balance toward harm when the role of oxidants in cell signaling pathways is suppressed [99]. Experimental research suggests protective effects through modulation of protein kinases [100, 101] and transcription factors [102-105]. [...]numerous preclinical studies have demonstrated that manipulation of chemokines, cytokines [13, 106], growth factors [107], receptors [108-110], and DAMPs [11, 12, 111] may limit hyperoxia-induced injury, but these targets all remain to be evaluated at the bedside.