Special Issue "TRP Channels in Health and Disease"
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: 31 December 2018
Transient receptor potential (TRP) channels represent an extended family of 28 members fulfilling multiple roles in the living organism. Over the last few years, new findings on TRP channels reveal an exceptionally broad spectrum as cellular sensors and effectors. Body temperature control, transmitter release from neurons, mineral homeostasis, chemical sensing, and survival mechanisms in a challenging environment are only a few functions which are tightly controlled by these channels. More than 20 hereditary human diseases in areas as diverse as neurology, cardiology, pulmonology, nephrology, dermatology, and urology caused by mutations in 11 TRP genes emphasize their truly remarkable diversity and underscore their essential role in vivo. Moreover, TRP channels are important pharmacological targets for specific novel therapeutic treatment options for patients suffering from diseases caused by dysfunctional TRP proteins. Along these lines, specific TRP inhibitors and activators were identified in the lasts years and are now tested in vitro and in vivo. At the cellular level, TRP channels can be activated by diverse chemical and physical stimuli and are involved in the regulation of the influx of external Ca2+—a universal second messenger regulating diverse cellular functions. However, TRP proteins do not function in isolation, but are organized as structural and functional protein modules in complex signal transduction pathways to execute essential tasks of the cell which are still under investigation. This special issue of Cells will feature a collection of excellent review articles summarizing the current state of the art on TRP channel research with a main focus on TRP channel activation, their physiological and pathophysiological function, and their roles as pharmacological targets for future therapeutic options.
Prof. Dr. Alexander Dietrich
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- TRP channels
- TRP function on an organismal, cellular, and molecular level
- TRPs and pathophysiological function
- TRP modulators as new therapeutic options
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Affiliation: Università Vita Salute San Raffaele, via Olgettina 58, 20132, Milan, Italy.
Tentative title: TRPC6 and inflammation: a growing stream in the landscape of elementary immunology
Abstract:Allergy and autoimmune diseases are characterised by the dysregulation of the immune response and by a multifactorial pathogenic background. Several genes involved in the control of key mechanisms for the deployment of innate and adaptive immunity have been progressively associated with the development of selected diseases and variably combine one with each other as well as with environmental factors to shape the characteristics of each individual’s manifestations. Among environmental factors, systemic or local perturbations in salt/water balance and in ion exchanges between the intra- and extracellular space or among tissues are growingly recognised as drivers of the immune response. In the setting of this research field, usually referred to as elementary immunology, novel evidence has been recently acquired on the potential role of the canonical transient receptor channel 6 (TRPC6) and its calcium/sodium currents in several inflammatory mechanisms. In fact, TRPC6 has been shown to be required for human leukocyte extravasation and murine neutrophil chemotaxis. Recent data also suggest that TRPC6 modulation can affect cytokine secretion and the likelihood of progression to apoptosis in human leukocytes. Accordingly, clinical evidence shows that genetic variants of TRPC6 affect the risk of selected inflammatory manifestations in patients with systemic lupus erythematosus, a prototypic autoimmune disorder, and that inhibition of TRPC6 might reduce the extent of airway responsiveness in allergic patients. Besides trimming the activity of immune cells, TRPC6 has also been shown to affect tissue susceptibility to inflammation and in particular to ischemia-reperfusion injury and excitotoxicity. Here, we provide a comprehensive review of most recent literature on the role of TRPC6 in the setting of immune-mediated diseases and discuss its potential pathogenic and therapeutic implications.