The development of our knowledge on the structure, molecular regulation, and cell function on transient receptor potential (TRP) channels has been growing dramatically during the last few years. Many meetings in the past and upcoming events are now focused on TRP channels as general sensor molecules in cell physiology. However, most of the scientists in the field still feel that we are just beginning to understand these truly remarkable proteins, called TRPs, and there is still a long way to go from structure via molecular regulation to cell and organ function. This generally accepted but exciting view about the long road to the understanding of TRPs dominated all presentations given at the 2006 Minerva-Gentner Symposium on TRP channels and calcium signalling, which was held in Eilat, Israel, and was excellently organized by Baruch Minke (Jerusalem, Israel) and supported by Veit Flockerzi (Homburg, Germany).
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http://dx.doi.org/10.1016/j.molcel.2006.04.015 | DOI Listing |
Heliyon
January 2025
Department of Oral Biology, Faculty of Dentistry, Mahidol University, Bangkok, Thailand.
Transient Receptor Potential (TRP) channels are a family of ion channels that play pivotal roles in various physiological processes, including sensory transduction, temperature regulation, and inflammation. In the context of dentistry, recent research has highlighted the involvement of TRP channels in mediating sensory responses and inflammation in dental tissues and temporo-mandibular joint (TMJ) structure. TRP channels have emerged as major contributors in the development of inflammatory conditions and pain affecting the oral cavity and related structures, such as periodontitis, dental erosion cause hypersensitivity, pulpitis, and TMJ disorders.
View Article and Find Full Text PDFEur J Pharmacol
January 2025
Graduate Program in Pharmacology, Federal University of Santa Catarina (UFSC), 88037-000 - Florianópolis (SC), Brazil. Electronic address:
Dithranol is one of the most effective topical medications for treating plaque psoriasis. However, its clinical use is limited by irritative adverse reactions to the skin, such as oedema, erythema, and pruritus, caused by poorly understood mechanisms. Because TRPV1 activation mediates skin irritation caused by several drugs, we conducted blind and randomised experiments in male and female C57BL/6 mice to elucidate the role of TRPV1 in dithranol-induced irritation.
View Article and Find Full Text PDFBackground And Purpose: Polycystins (PKD2, PKD2L1) are voltage-gated and Ca -modulated members of the transient receptor potential (TRP) family of ion channels. Loss of PKD2L1 expression results in seizure-susceptibility and autism-like features in mice, whereas variants in PKD2 cause autosomal dominant polycystic kidney disease. Despite decades of evidence clearly linking their dysfunction to human disease and demonstrating their physiological importance in the brain and kidneys, the polycystin pharmacophore remains undefined.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Pain Management, The State Key Specialty in Pain Medicine, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Background: The nod-like receptor family pyrin domain-containing 3 (NLRP3) has been implicated in various skin diseases. However, its role in mediating 2, 4-dinitrofluorobenzene (DNFB)-induced chronic itch remains unclear.
Methods: Widetype () and deletion ( )mice, the expression of transient receptor potential (TRP) ankyrin 1 (TRPA1) inhibitor or recombinant mice interleukin-18 (IL-18) were used to establish and evaluate the severity of DNFB-mediated chronic itch.
Int J Mol Sci
January 2025
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
Pulmonary hypertension associated with lung diseases and/or hypoxia is classified as group 3 in the clinical classification of pulmonary hypertension. The efficacy of existing selective pulmonary vasodilators for group 3 pulmonary hypertension is still unknown, and it is currently associated with a poor prognosis. The mechanisms by which pulmonary hypertension occurs include hypoxic pulmonary vasoconstriction, pulmonary vascular remodeling, a decrease in pulmonary vascular beds, endothelial dysfunction, endothelial-to-mesenchymal transition, mitochondrial dysfunction, oxidative stress, hypoxia-inducible factors (HIFs), inflammation, microRNA, and genetic predisposition.
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