Title: TRPV1 Function in Health and Disease
Volume: 12
Issue: 1
Author(s): John P.M. White, Laszlo Urban and Istvan Nagy
Affiliation:
Keywords:
Vanilloid, capsaicin, TRPV1, pain, inflammation, neuropathy, peripheral nervous system, central nervous system, sensitisation, bradykinin, prostaglandins, nerve growth factor, hyperalgesia, resiniferatoxin, perikarya, hepatoblastoma, periaqueductal gray, anti-nociceptive effects, mu-opioid receptors, Inflammatory mediators, endothelin, muscle nociception, allodynia, tissue acidosis, cancer metastasis, cardiogenic sympathoexcitatory, synovial membrane, osteoarthritis, rheumatoid arthritis, capsazepine
Abstract: The transient receptor potential vanilloid type 1 ion channel (TRPV1) was identified as a receptor responsible for mediating the intense burning sensation following exposure to heat greater than ∼43 °C, or to capsaicin, the pungent ingredient of hot chilli peppers. More importantly, however, it has been shown that TRPV1 plays a pivotal role in the development of the burning pain sensation associated with inflammation in peripheral tissues. More recently, there has been a virtual avalanche of sightings of TRPV1 on the anatomical landscape, coupled with association of TRPV1 with a wide range of non-pain-related physiological and pathological conditions. Here, we consider the continuously expanding set of functions in both health and disease which TRPV1 is understood to subserve at present. The widespread expression of TRPV1 in the human suggests that, in addition to the development of burning pain associated with acute exposure to heat or capsaicin, and with inflammation, TRPV1 may also be involved in an array of vitally important functions, such as those of the urinary tract, the respiratory and auditory systems. Moreover, TRPV1 may also be involved in the maintenance of body and cell homeostasis, metabolism, regulation of hair growth, and development of cancer. Thus, controlling TRPV1 function may possess the potential of providing exciting opportunities for therapeutic interventions. At the same time, however, the widespread distribution of these ion channels introduces a tremendous complication in developing a drug to serve in one disease context which may have profound implications for normal TRPV1 functioning in other non-pathological contexts.
