Reactive oxygen species and angiogenesis: NADPH oxidase as target for cancer therapy.

By M. Ushio-Fukai, Yoshimasa Nakamura. Cancer Letters, 2008

636 citations recorded by the source corpus.

Subfields: Biomedical Engineering, Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/31682f9a2121c3245b3b3acc2133f33dce55686b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biomedical Engineering

1. Subash C. Gupta
2. Jing Yi
3. Jie Wang
4. S. Dikalov

In Cancer Research

1. Subash C. Gupta
2. Gautam Sethi
3. Jing Yi
4. Bharat B. Aggarwal
5. Jie Wang
6. S. Dikalov

In Molecular Biology

1. Subash C. Gupta
2. Sridevi Patchva
3. Bharat B. Aggarwal
4. Gautam Sethi
5. Wonil Koh
6. Jing Yi
7. Jie Wang
8. S. Dikalov

Citations in the corpus

• Erk2 phosphorylation of Drp1 promotes mitochondrial fission and MAPK-driven tumor growth (2015, background): “We speculate that MAPK-induced mitochondrial fission may promote the activation of proangiogenic signaling pathways, which are known to be sensitive to mitochondria-derived reactive oxygen species (Ushio-Fukai and Nakamura, 2008; Xia et al., 2007).”
• Upsides and Downsides of Reactive Oxygen Species for Cancer: The Roles of Reactive Oxygen Species in Tumorigenesis, Prevention, and Therapy (2012, positive): “Accumulating evidence over the past several years from both in vitro and in vivo studies has indicated a role for ROS as a signaling mediator of angiogenesis and metastasis (306– 308).”
• Crosstalk between mitochondria and NADPH oxidases (2011, background): “Recent progress on the role of ROS derived from NADPH oxidases and redox signaling events involved in angiogenesis implicates NADPH oxidases as potential therapeutic targets for tumor angiogenesis [139].”
• Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements (2019, background): “Both endogenous and exogenous ROS spearheads stimulation of growth factors, cytokines, and transcription factors like VEGF and HiF-1α, which promote tumor migration and proliferation through ROS-dependent cellular signaling [62,65,66].”
• Cancer cell killing via ROS: To increase or decrease, that is the question (2008, methodology): “(1) TrxR and Trx overexpression have been reported in several malignancies and may be associated with aggressive tumor growth, poor survival and resistance to chemotherapy.”