Reactive oxygen and mechanisms of inflammatory liver injury: Present concepts

By H. Jaeschke. Journal of Gastroenterology and Hepatology, 2011

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Oxidative Stress and Air Pollution Exposure (2011, background): “The additional release of cell contents amplifies the inflammatory process and consequently can induce tissue injury [20].”
Reperfusion injury and reactive oxygen species: The evolution of a concept (2015, neutral): “).”
Decoding cell death signals in liver inflammation. (2013, background): “Hypoxia induces indeed a considerable overgeneration of ROS [78], in turn (i) directly stimulating the (at least partially) NF-jB-dependent transactivation of various proinflammatory mediators [53] and (ii) promoting protein unfolding and hence triggering the ER stress response (as documented by the”
Dietary cholesterol drives fatty liver-associated liver cancer by modulating gut microbiota and metabolites (2020, background): “19 Indeed, our analysis revealed that dietary cholesterol induced both ROS and proinflammatory cytokines, thereby promoting NASH and HCC development.”
OXIDANT STRESS, MITOCHONDRIA AND CELL DEATH MECHANISMS IN DRUG-INDUCED LIVER INJURY: LESSONS LEARNED FROM ACETAMINOPHEN HEPATOTOXICITY (2012, background): “However, LPO products are biomarkers for oxidant stress (Guéraud et al., 2010; Jaeschke, 2011), and they can act as signaling molecules by modifying proteins or DNA within the cell or can act as chemotactic agents (Dianzani, 2003; Jaeschke, 2011; Marnett, 2002; Negre-Salvayre et al.”