Cholinergic agonists inhibit HMGB1 release and improve survival in experimental sepsis
By Hong Wang, H. Liao, M. Ochani, Marilou Justiniani, Xinchun Lin, Lihong Yang, Y. Al-Abed, Haichao Wang, C. Metz, E. Miller and 2 more. Nature Medicine, 2004
1,199 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/fcef92fe7df0670524ba8a6beb63c9a4828e3e60
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Clinical Biochemistry
In Molecular Biology
- Kevin J. Tracey
- C. Deutschman
- Valentin A. Pavlov
- Michael Lotze
- Luis Ulloa
- M. Ochani
- W. Jonge
- U. Andersson
In Neurology
- Kevin J. Tracey
- C. Deutschman
- Valentin A. Pavlov
- Luis Ulloa
- W. Jonge
- M. Ochani
- C. Czura
- M. Rosas‐Ballina
Citations in the corpus
- Sepsis: current dogma and new perspectives. (2014, background): “Serum HMGB1 accumulation in response to infection or injury is nearly universally found in animal studies and clinical investigations of severe sepsis Immunity 40, April 17, 2014 ª2014 Elsevier Inc. 469 (Angus et al., 2007; Andersson and Tracey, 2011; Wang et al., 2004; Wang et al., 2004).”
- High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal (2005, background): “Nicotine and acetylcholine inhibit both endotoxin- and TNF-induced HMGB1 release in vitro and in vivo , thereby reducing serum HMGB1 levels and improving survival in mouse models of sepsis, which indicates that targeting the nicotinic receptor in the peripheral nervous system could have therapeut”
- Splenectomy inactivates the cholinergic antiinflammatory pathway during lethal endotoxemia and polymicrobial sepsis (2006, methodology): “Previously, the survival benefi ts of nicotine were found to correlate with reduced serum levels of HMGB1, a necessary and suffi cient mediator of lethal systemic infl ammation (11).”
- HMGB1 Is a Therapeutic Target for Sterile Inflammation and Infection (2011, background): “Decreased release due to nuclear retention (35, 36)”
- The alpha7 nicotinic acetylcholine receptor as a pharmacological target for inflammation (2007, background): “In different cell types including monocytes, macrophages and endothelial cells, studies have indicated that the antiinflammatory potential of the a7-nAChR is mediated by the inhibition of the transcription factor, NF-kB (Sugano et al., 1998; Wang et al., 2004; Saeed et al., 2005).”