Reactive oxygen species, cell signaling, and cell injury.

By K. Hensley, K. Robinson, S. Gabbita, S. Salsman, R. Floyd. Free Radical Biology & Medicine, 2000

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Pathophysiology of Myocardial Infarction (2015, positive): “ROS promote leukocyte chemotaxis (141) by activating complement, by stimulating expression of P-selectin and by upregulating cytokine and chemokine synthesis through activation of the nuclear factor (NF)-κB system (156).”
Pre-eclampsia, the placenta and the maternal systemic inflammatory response--a review. (2003, neutral): “arable phenomena (Hensley et al., 2000).”
Alcohol-induced oxidative stress. (2007, background): “NF-κB is activated upon phosphorylation of an inhibitory subunit (IκB) (Hensley et al., 2000) with the help of ATP.”
Oxidative Stress in Obesity: A Critical Component in Human Diseases (2014, background): “The main element of NAFLD is the accumulation of TG as fat droplets within the cytoplasm of hepatocytes, which is a prerequisite for subsequent events of NASH.”
Oxygen, oxidative stress, hypoxia, and heart failure. (2005, background): “ROS have an important role in several important biological processes, including the oxidative burst reaction essential to phagocytes (27).”
Antioxidant Properties of Probiotic Bacteria (2017, background): “Subsequently, some other transcription factors and kinases, including hypoxia-inducible factors (HIFs) and phosphatidylinositol 3-kinase (PI3K), have been discovered to possess redox-sensitive elements that can be regulated by ROS [1,20].”