TRPA1 is a Ca2+-permeable non-selective cation channel with reported values of PCa2+/PNa+ between 0.8 and 7.9 [
45,
46,
47]. This channel is activated by a large number of irritants found in plants, food, cosmetics and pollutants [
48]. Several TRPA1 agonists are highly reactive electrophiles with a shared ability to modify covalently cysteine and lysine residues in the N-terminus of the channel [
49,
50]. Examples of electrophilic activators are allyl isothiocyanate (found in wasabi and mustard), cinnamaldehyde (in cinnamon), nicotine (in formulations of smoking cessation therapies), and acrolein (in exhaust gasses) [
51,
52,
53,
54]. TRPA1 functions as a chemosensor in sensory tissues involved in innate defence mechanisms, thereby contributing to the organism’s integrity [
55,
56]. Activation of TRPA1 in sensory neurons produces acute pain [
52], thermal and mechanical hyperalgesia, and more general, inflammatory pain [
51]. As such, TRPA1 is involved in various molecular pathways leading to inflammatory pain.
TRPA1 is expressed in numerous tissues throughout the body. Sensory neurons of the vagal, nodose, trigeminal and dorsal root ganglia express TRPA1 in unmyelinated C-fibers and myelinated Aδ-fibers, both in peptidergic and non-peptidergic neurons. TRPA1 expression was also reported in non-excitable cells, such as epithelial cells, fibroblasts [
57], pancreatic islet cells, several cell types in the gastrointestinal tract [
58,
59,
60], vascular endothelial cells [
61] and several cell types in the respiratory tract [
62,
63]. This heterogeneous distribution of TRPA1 suggests its potential implications in physiological functions and pathological conditions, within and beyond the nervous system.
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