Genetic ablation of Nrf2 enhances susceptibility to cigarette smoke-induced emphysema in mice.

By T. Rangasamy, C. Cho, R. Thimmulappa, Lijie Zhen, S. Srisuma, T. Kensler, Masayuki Yamamoto, I. Petrache, R. Tuder, Shyam Biswal. Journal of Clinical Investigation, 2004

995 citations recorded by the source corpus.

Subfields: Health, Toxicology and Mutagenesis, Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/518c46ae48eac595838fafe54807f982ee485cd0

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In Health, Toxicology and Mutagenesis

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In Pulmonary and Respiratory Medicine

Donna D. Zhang

Citations in the corpus

Mechanistic Studies of the Nrf2-Keap1 Signaling Pathway (2006, background): “Nrf2 downstream genes can be classified into categories according to their functions: cellular redox homeostasis, cell growth and apoptosis, inflammatory response, and the ubiquitin-mediated degradation pathway (Thimmulappa et al., 2002; Kwak et al., 2003; Lee et al., 2003; Rangasamy et al., 2004; C”
Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis. (2006, methodology): “tissue or cells by using the protocol described previously (7).”
The Impact of Oxidative Stress and Inflammation on RPE Degeneration in Non-neovascular AMD (2017, background): “The macula lives in a high oxidative stress environment, which can be magnified by those who choose to smoke, making it the strongest non-genetic risk factor for AMD aside from chronological aging (Rahman and MacNee, 1996; Rangasamy et al., 2004; Smith and Hansch, 2000).”
How cigarette smoke skews immune responses to promote infection, lung disease and cancer (2009, background): “; variation in genes involved in the DNA damage response and DNA repai”
Global mapping of binding sites for Nrf2 identifies novel targets in cell survival response through ChIP-Seq profiling and network analysis (2010, methodology): “WT and Nrf2 / male mice (CD-1 strain, 8–10weeks) were exposed to CS for 5 h/day using a TE-10 smoking machine (Teague Enterprises, Davis, CA) and 3R4F reference cigarettes (University of Kentucky, Tobacco Research Institute, Lexington, KY) as described previously (8).”
The cytoprotective role of the Keap1–Nrf2 pathway (2011, background): “…diesel exhaust fumes, dimethylbenz(a)anthracene, cigarette smoke, dextran sulphate, 3-nitropropionic acid and malonate (Chan and Kan 1999; Enomoto et al. 2001; Aoki et al. 2001; Ramos-Gomez et al. 2002; Xu et al. 2006; Rangasamy et al. 2004; Calkins et al. 2005; Khor et al. 2006; 2008).”
Role of nrf2 in oxidative stress and toxicity. (2013, background): “Cigarette Smoke and COPD Chronic exposure to cigarette smoke in the lungs is typically associated with the development of COPD (in particular, emphysema) and lung cancer.”
Disruption of Nrf2 enhances susceptibility to severe airway inflammation and asthma in mice (2005, background): “Our recent study (28) revealed the importance of 50 Nrf2-dependent antioxidant and cytoprotective genes in the protection of lungs against cigarette smoke–induced emphy-”
Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease (2015, positive): “The common themes associated with these conditions are inflammation and oxidative stress; it has been shown previously that loss of Nrf2 increases sensitivity to oxidative insults and proinflammatory stimuli, indicating that Nrf2 is likely to play a significant role in many neurodegenerative conditi”
Inflammation, a Key Event in Cancer Development (2006, background): “NF-nB Mediate inflammation progress, promoting chronic inflammation (134, 135, 142) Promote the production of mutagenic reactive oxygen species (128) Protect transformed cells from apoptosis (157, 158) Promote tumor invasion and metastasis (5, 160) Feedback loop between proinflammatory cytokines (13”