Trpa1, short for transient receptor potential ankyrin 1, is a nonselective cation channel permeable to Ca(2+), Na(+), and K(+). It functions as a promiscuous chemical nocisensor involved in noxious cold and mechanical sensation [3]. Present in nociceptive sensory neurons and other cells, in primary sensory neurons, its activation leads to membrane depolarization, action potential discharge, and neurotransmitter release [3]. It is also associated with pathways related to pain, inflammation, and temperature sensation, and is of great biological importance in these processes [1,2,4,6]. Genetic models like KO/CKO mouse models are valuable for studying its functions.

Preclinical evidence from murine models of pain diseases indicates that multiple mechanisms converge on the pathway involving oxidative stress and Schwann cell Trpa1 to sustain chronic pain [1]. These models suggest that Trpa1 has a role in chronic pain conditions, making it a potential therapeutic target for pain relief [1]. In immune cells, although functional measurements are scarce, Trpa1 has been linked to diseases like arthritis, anaphylaxis, and inflammatory bowel disease, suggesting its involvement in immune-related pathologies [5].

In conclusion, Trpa1 is crucial for chemo -, thermo -, and mechano-sensing in nociceptive neurons and has a dual role in immunity [5]. Mouse models, especially KO/CKO models, have revealed its significance in chronic pain and immune-related disease areas, highlighting its potential as a therapeutic target for treating conditions such as chronic pain, itch, sensory hyperreactivity in visceral organs, and certain inflammatory diseases [1,3,5].