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However, when the adaptive capacity is overcome, hemolytic erythrocyte-derived products act as signaling molecules, namely DAMPs, which promote inflammation via triggering TLR4-dependent activation of endothelial cells associated with NF-B-mediated synthesis of proinflammatory cytokines, TLR4-independent, ROS-, NADPH oxidase- and heme iron-mediated promotion of neutrophil extracellular traps (NETs) formation, TLR4-dependent activation of macrophages accompanied by secretion of tumor necrosis factor (TNF-), and MyD88/TRIF pathway-mediated TLR4-dependent microglia activation that triggers neuroinflammation [224]
Kim KS, Park JS, Hwang E, Park MJ, Shin HY, Lee YH, et al
Dastghaib S, Shojaei S, Mostafavi-Pour Z, Sharma P, Patterson JB, Samali A, et al
Moreover, chronic intermittent hypoxia, a hallmark of OSAS, contributes to endothelial dysfunction and the progression of atherosclerosis, thus significantly increasing the risk of hypertension, stroke, and myocardial infarction [9]
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