Oxygen sensing by mitochondria at complex III: the paradox of increased reactive oxygen species during hypoxia

By R. Guzy, P. Schumacker. Experimental Physiology, 2006

901 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8a161aefb702aba58dca0830e34247b68c682ae7

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Citations in the corpus

Flooding stress: acclimations and genetic diversity. (2008, background): “Under normoxia, PHDs target the proteosomal degradation of hypoxia inducible factor 1α (HIF1α), a subunit of a heterodimeric transcription factor that regulates acclimation to hypoxia (51).”
Hypoxia and metabolism: Hypoxia, DNA repair and genetic instability (2008, background): “Exposure to cycling hypoxia can lead to increased levels of reactive oxygen species (ROS) in the cell, in part owing to increased release of such species from mitochondri”
Mitochondrial electron transport chain: Oxidative phosphorylation, oxidant production, and methods of measurement (2020, background): “As described above, the two electrons carried by QH2 when it binds Complex III are transferred from QH2 to the Rieske Fe–”
Reactive oxygen species and mitochondria: A nexus of cellular homeostasis (2015, background): “Depending on the context and triggering stimuli, mtROS production can lead to different cellular responses such as cellular adaptation to hypoxia [43], cellular differentiation [44], autophagy [5], inflammation [45], or an immune response [6].”
How mitochondria produce reactive oxygen species (2008, background): “These studies have led to the proposal that the source of the ROS is complex III [121], possibly a ubisemiquinone at the Q o site [126] , thereby altering the P R of protein redox groups.”
Mitochondria in cancer cells: what is so special about them? (2008, positive): “However, ROS levels can also be increased by hypoxia, when electron transport complexes are in the reduced state [ 31 ].”
Fatty acid uptake and lipid storage induced by HIF-1α contribute to cell growth and survival after hypoxia-reoxygenation. (2014, positive): “Mitochondrial ROS production increases in hypoxia (Guzy et al., 2005; Guzy and Schumacker, 2006).”
How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis). (2010, background): “…mitochondrial compartment to other compartments of the cell (Barja, 1993; Rhee et al., 2003; Kaelin, 2005; Connor et al., 2005; Guzy et al., 2005; Guzy and Schumacker, 2006; Chandel and Budinger, 2007; Schulz et al., 2007; Veal et al., 2007; Owusu-Ansah et al., 2008; Finley and Haigis, 2009;…”
Pathophysiology of placental‐derived fetal growth restriction (2018, background): “However, generation of ROS is increased during hypoxia and ischemiareperfusion, when buildup of electrons on the electron transport chain leads to a greater rate of leakage.(63) Thus, exposure of placental explants to cycles of hypoxia-reoxygenation is a powerful generator of oxidative stress, induc”