4-Hydroxynonenal, an endogenous aldehyde, causes pain and neurogenic inflammation through activation of the irritant receptor TRPA1
By M. Trevisani, J. Siemens, Serena Materazzi, D. Bautista, R. Nassini, B. Campi, N. Imamachi, E. André, R. Patacchini, G. Cottrell and 5 more. Proceedings of the National Academy of Sciences of the United States of America, 2007
779 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Physiology, Sensory Systems
View Paper: https://www.semanticscholar.org/paper/f00b982419ebe98850c51bf10d802cfa2a7bd52e
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
In Physiology
In Sensory Systems
Citations in the corpus
- TRP channels and pain. (2013, background): “TRPA1 is also activated by endogenous products of oxidative or nitrative stress, such as 4-hydroxynonenal, which is produced when reactive oxygen species peroxidate membrane lipids (Andersson et al. 2008, Trevisani et al. 2007).”
- TRP Channels (2012, neutral): “Furthermore TRPA1 is also activated by endogenous substances such as 4-hydroxynonenal and 15-deoxy-(cid:2) 12,14-prostaglandin J2, which are released after inflammation, oxidative stress, or tissue damage (22,254,405,418).”
- Transient Receptor Potential A1 Is a Sensory Receptor for Multiple Products of Oxidative Stress (2008, positive): “These results are consistent with the independent previous reports by two other groups that 4-HNE activates TRPA1 (Macpherson et al., 2007b; Trevisani et al., 2007).”
- Enterochromaffin Cells Are Gut Chemosensors that Couple to Sensory Neural Pathways. (2017, positive): “such as 4-hydroxynonenal, prostaglandins and other lipid-derived metabolites (Bautista et al., 2006; Trevisani et al., 2007).”
- Cellular and Molecular Mechanisms of Pain (2009, neutral): “…such agents are 4-hydroxy-2nonenal and 15-deoxy-∆12,14-prostaglandin J2, which are both a,β unsaturated aldehydes generated through peroxidation or spontaneous dehydration of lipid second messengers (Andersson et al., 2008; Cruz-Orengo et al., 2008; Materazzi et al., 2008; Trevisani et al., 2007).”