Regulation of Autophagy by Reactive Oxygen Species (ROS): Implications for Cancer Progression and Treatment
By M. Azad, Yongqiang Chen, S. Gibson. Antioxidants and Redox Signaling, 2009
752 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/65ab6afab79b4f4101e7b6d45a4a474c3ea7a6a1
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Citations in the corpus
- The Impact of Oxidative Stress and Inflammation on RPE Degeneration in Non-neovascular AMD (2017, background): “Oxidative stress induces a cellular antioxidant response, including in RPE cells, which has been linked to activation of autophagy through the p62/Keap1/Nrf2 pathway (Azad et al., 2009; Filomeni et al., 2010; Johansson et al., 2015; Wang et al., 2014a).”
- Oxidative stress, inflammation, and cancer: how are they linked? (2010, background): “ROS have also been reported to activate Akt by inhibiting phosphatase and tensin homolog deleted from chromosome10 (PTEN), the phosphatase counteracting PI3K-dependent Akt activation [167].”
- Upsides and Downsides of Reactive Oxygen Species for Cancer: The Roles of Reactive Oxygen Species in Tumorigenesis, Prevention, and Therapy (2012, neutral): “Studies during the past 5 years have indicated a role for ROS as a signaling molecule in inducing autophagic cell death in cancer cells (20, 97, 139).”
- Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging (2011, background): “It is generally accepted that ROS induce autophagy [125, 126], and that autophagy, in turn, serves to reduce oxidative damage [124].”