Fig. 5
From: Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome
Schematic demonstrating the central role played by oxidative stress and inflammation in OSAS. OSAS/IH induces ROS production by inducing mitochondrial dysfunction, activating NOX and XOX, and inducing NOS uncoupling, which results in oxidative stress. The interaction between ROS and NO further promotes oxidative stress and diminishes the bioavailability of NO, thus promoting endothelial dysfunction and inflammation, which is closely related to hypertension, atherosclerosis, and hypercoagulability. Increased ROS-dependent sympathetic activation enhances renin levels, which leads to an increase in angiotensin II, endothelin 1, and hypertension. As a second messenger, ROS can activate multiple signaling pathways (MAPK, JNK), which in turn activate NF-κB and then induce the activation of nuclear transcription factors in a variety of cells. As the main switch of the inflammatory response, NF-κB plays an important role in the pathological process of OSAS, activating and entering the nucleus, regulating the transcription of many kinds of cells (immune cells), causing an increase in cytokines and participating in the inflammatory process of cells. In addition, elevated ROS can damage intracellular macromolecular substances (DNA) and cause cell death. Various pathological processes coordinate with each other and induce low-grade inflammation in the body, which is closely related to the occurrence and progression of a variety of diseases. ROS reactive oxygen species, NOX NADPH oxidase, NOS uncoupling nitric oxide synthase uncoupling, XOX xanthine oxidase, NOS nitric oxide synthase, JNK c‐Jun N‐terminal kinase, MAPK mitogen-activated protein kinase, NF-κB nuclear factor kappa B
