Special Issue "TRP Channels in Health and Disease"

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 December 2018

Special Issue Editor

Guest Editor
Prof. Dr. Alexander Dietrich

Walther-Straub-Institute of Pharmacology and Toxicology, Ludwig-Maximilians-Universitat Munchen, Munich, Germany
Website | E-Mail
Interests: TRP channels; lung physiology and pathophysiology; TRP-deficient mouse models; TRP modulators as therapeutic options

Special Issue Information

Dear Colleagues,

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
Guest Editor

Manuscript Submission Information

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Keywords

  • TRP channels
  • TRP function on an organismal, cellular, and molecular level
  • TRPs and pathophysiological function
  • TRP modulators as new therapeutic options

Published Papers (11 papers)

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Research

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Open AccessArticle Transient Receptor Potential Channel A1 (TRPA1) Regulates Sulfur Mustard-Induced Expression of Heat Shock 70 kDa Protein 6 (HSPA6) In Vitro
Received: 26 July 2018 / Revised: 23 August 2018 / Accepted: 28 August 2018 / Published: 31 August 2018
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Abstract
The chemosensory transient receptor potential ankyrin 1 (TRPA1) ion channel perceives different sensory stimuli. It also interacts with reactive exogenous compounds including the chemical warfare agent sulfur mustard (SM). Activation of TRPA1 by SM results in elevation of intracellular calcium levels but the
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The chemosensory transient receptor potential ankyrin 1 (TRPA1) ion channel perceives different sensory stimuli. It also interacts with reactive exogenous compounds including the chemical warfare agent sulfur mustard (SM). Activation of TRPA1 by SM results in elevation of intracellular calcium levels but the cellular consequences are not understood so far. In the present study we analyzed SM-induced and TRPA1-mediated effects in human TRPA1-overexpressing HEK cells (HEKA1) and human lung epithelial cells (A549) that endogenously exhibit TRPA1. The specific TRPA1 inhibitor AP18 was used to distinguish between SM-induced and TRPA1-mediated or TRPA1-independent effects. Cells were exposed to 600 µM SM and proteome changes were investigated 24 h afterwards by 2D gel electrophoresis. Protein spots with differential staining levels were analyzed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and nano liquid chromatography electrospray ionization tandem mass spectrometry. Results were verified by RT-qPCR experiments in both HEKA1 or A549 cells. Heat shock 70 kDa protein 6 (HSPA6) was identified as an SM-induced and TRPA1-mediated protein. AP18 pre-treatment diminished the up-regulation. RT-qPCR measurements verified these results and further revealed a time-dependent regulation. Our results demonstrate that SM-mediated activation of TRPA1 influences the protein expression and confirm the important role of TRPA1 ion channels in the molecular toxicology of SM. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
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Open AccessArticle GABAB Receptors Augment TRPC3-Mediated Slow Excitatory Postsynaptic Current to Regulate Cerebellar Purkinje Neuron Response to Type-1 Metabotropic Glutamate Receptor Activation
Received: 26 May 2018 / Revised: 18 July 2018 / Accepted: 27 July 2018 / Published: 29 July 2018
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Abstract
During strong parallel fiber stimulation, glutamate released at parallel fiber-Purkinje cell synapses activates type-1 metabotropic glutamate receptor (mGluR1) to trigger a slow excitatory postsynaptic current (sEPSC) in cerebellar Purkinje neurons. The sEPSC is mediated by transient receptor potential canonical 3 (TRPC3) channels. Often
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During strong parallel fiber stimulation, glutamate released at parallel fiber-Purkinje cell synapses activates type-1 metabotropic glutamate receptor (mGluR1) to trigger a slow excitatory postsynaptic current (sEPSC) in cerebellar Purkinje neurons. The sEPSC is mediated by transient receptor potential canonical 3 (TRPC3) channels. Often co-localized with mGluR1 in Purkinje neuron dendrites are type B γ-aminobutyric acid receptors (GABABRs) that respond to inhibitory synaptic inputs from interneurons located in the molecular layer of cerebellar cortex. It has been shown that activation of postsynaptic GABABRs potentiates mGluR1 activation-evoked sEPSC in Purkinje cells, but the underlying molecular mechanism remains elusive. Here we report that the augmentation of mGluR1-sEPSC by GABABR activation in Purkinje neurons is completely absent in TRPC3 knockout mice, but totally intact in TRPC1-, TRPC4-, and TRPC1,4,5,6-knockout mice, suggesting that TRPC3 is the only TRPC isoform that mediates the potentiation. Moreover, our results indicate that the potentiation reflects a postsynaptic mechanism that requires both GABABRs and mGluR1 because it is unaffected by blocking neurotransmission with tetrodotoxin but blocked by inhibiting either GABABRs or mGluR1. Furthermore, we show that the co-stimulation of GABABRs has an effect on shaping the response of Purkinje cell firing to mGluR1-sEPSC, revealing a new function of inhibitory input on excitatory neurotransmission. We conclude that postsynaptic GABABRs regulate Purkinje cell responses to strong glutamatergic stimulation through modulation of mGluR1-TRPC3 coupling. Since mGluR1-TRPC3 coupling is essential in cerebellar long-term depression, synapse elimination, and motor coordination, our findings may have implications in essential cerebellar functions, such as motor coordination and learning. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
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Open AccessArticle TRPV1-Like Immunoreactivity in the Human Locus K, a Distinct Subregion of the Cuneate Nucleus
Received: 29 April 2018 / Revised: 30 June 2018 / Accepted: 5 July 2018 / Published: 8 July 2018
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Abstract
The presence of transient receptor potential vanilloid type-1 receptor (TRPV1)-like immunoreactivity (LI), in the form of nerve fibres and terminals, is shown in a set of discrete gray matter subregions placed in the territory of the human cuneate nucleus. We showed previously that
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The presence of transient receptor potential vanilloid type-1 receptor (TRPV1)-like immunoreactivity (LI), in the form of nerve fibres and terminals, is shown in a set of discrete gray matter subregions placed in the territory of the human cuneate nucleus. We showed previously that those subregions share neurochemical and structural features with the protopathic nuclei and, after the ancient name of our town, collectively call them Locus Karalis, and briefly Locus K. TRPV1-LI in the Locus K is codistributed, though not perfectly overlapped, with that of the neuropeptides calcitonin gene-related peptide and substance P, the topography of the elements immunoreactive to the three markers, in relation to each other, reflecting that previously described in the caudal spinal trigeminal nucleus. Myelin stainings show that myelinated fibres, abundant in the cuneate, gracile and trigeminal magnocellular nuclei, are scarce in the Locus K as in the trigeminal substantia gelatinosa. Morphometric analysis shows that cell size and density of Locus K neurons are consistent with those of the trigeminal substantia gelatinosa and significantly different from those of the magnocellular trigeminal, solitary and dorsal column nuclei. We propose that Locus K is a special component of the human dorsal column nuclei. Its functional role remains to be determined, but TRPV1 appears to play a part in it. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
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Open AccessArticle Expression Profiling of the Transient Receptor Potential Vanilloid (TRPV) Channels 1, 2, 3 and 4 in Mucosal Epithelium of Human Ulcerative Colitis
Received: 30 April 2018 / Revised: 11 June 2018 / Accepted: 14 June 2018 / Published: 15 June 2018
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Abstract
The Transient Receptor Potential (TRP) family of selective and non-selective ion channels is well represented throughout the mammalian gastrointestinal track. Several members of the Transient Receptor Potential Vanilloid (TRPV) subfamily have been identified in contributing to modulation of mobility, secretion and sensitivity of
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The Transient Receptor Potential (TRP) family of selective and non-selective ion channels is well represented throughout the mammalian gastrointestinal track. Several members of the Transient Receptor Potential Vanilloid (TRPV) subfamily have been identified in contributing to modulation of mobility, secretion and sensitivity of the human intestine. Previous studies have focused on the detection of TRPV mRNA levels in colon tissue of patients with inflammatory bowel disease (IBD) whereas little information exists regarding TRPV channel expression in the colonic epithelium. The aim of this study was to evaluate the expression levels of TRPV1, TRPV2, TRPV3 and TRPV4 in mucosa epithelial cells of colonic biopsies from patients with ulcerative colitis (UC) in comparison to colonic resections from non-IBD patients (control group). Immunohistochemistry, using specific antibodies and quantitative analyses of TRPV-immunostained epithelial cells, was performed in semi-serial sections of the samples. TRPV1 expression was significantly decreased whereas TRPV4 expression was significantly increased in the colonic epithelium of UC patients compared to patients in the control group (p < 0.05). No significant difference for TRPV2 and TRPV3 expression levels between UC and control specimens was detected (p > 0.05). There was no correlation between TRPV channel expression and the clinical features of the disease (p > 0.05). Further investigation is needed to clarify the role of TRPV channels in human bowel inflammatory response. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
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Review

Jump to: Research

Open AccessFeature PaperReview The Channel-Kinase TRPM7 as Novel Regulator of Immune System Homeostasis
Received: 13 July 2018 / Revised: 13 August 2018 / Accepted: 13 August 2018 / Published: 17 August 2018
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Abstract
The enzyme-coupled transient receptor potential channel subfamily M member 7, TRPM7, has been associated with immunity and immune cell signalling. Here, we review the role of this remarkable signalling protein in lymphocyte proliferation, differentiation, activation and survival. We also discuss its role in
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The enzyme-coupled transient receptor potential channel subfamily M member 7, TRPM7, has been associated with immunity and immune cell signalling. Here, we review the role of this remarkable signalling protein in lymphocyte proliferation, differentiation, activation and survival. We also discuss its role in mast cell, neutrophil and macrophage function and highlight the potential of TRPM7 to regulate immune system homeostasis. Further, we shed light on how the cellular signalling cascades involving TRPM7 channel and/or kinase activity culminate in pathologies as diverse as allergic hypersensitivity, arterial thrombosis and graft versus host disease (GVHD), stressing the need for TRPM7 specific pharmacological modulators. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
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Open AccessFeature PaperReview TRPs in Tox: Involvement of Transient Receptor Potential-Channels in Chemical-Induced Organ Toxicity—A Structured Review
Received: 29 May 2018 / Revised: 24 July 2018 / Accepted: 31 July 2018 / Published: 7 August 2018
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Abstract
Chemicals can exhibit significant toxic properties. While for most compounds, unspecific cell damaging processes are assumed, a plethora of chemicals exhibit characteristic odors, suggesting a more specific interaction with the human body. During the last few years, G-protein-coupled receptors and especially chemosensory ion
[...] Read more.
Chemicals can exhibit significant toxic properties. While for most compounds, unspecific cell damaging processes are assumed, a plethora of chemicals exhibit characteristic odors, suggesting a more specific interaction with the human body. During the last few years, G-protein-coupled receptors and especially chemosensory ion channels of the transient receptor potential family (TRP channels) were identified as defined targets for several chemicals. In some cases, TRP channels were suggested as being causal for toxicity. Therefore, these channels have moved into the spotlight of toxicological research. In this review, we screened available literature in PubMed that deals with the role of chemical-sensing TRP channels in specific organ systems. TRPA1, TRPM and TRPV channels were identified as essential chemosensors in the nervous system, the upper and lower airways, colon, pancreas, bladder, skin, the cardiovascular system, and the eyes. Regarding TRP channel subtypes, A1, M8, and V1 were found most frequently associated with toxicity. They are followed by V4, while other TRP channels (C1, C4, M5) are only less abundantly expressed in this context. Moreover, TRPA1, M8, V1 are co-expressed in most organs. This review summarizes organ-specific toxicological roles of TRP channels. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
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Open AccessFeature PaperReview TRPC3 as a Target of Novel Therapeutic Interventions
Received: 10 June 2018 / Revised: 18 July 2018 / Accepted: 20 July 2018 / Published: 22 July 2018
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Abstract
TRPC3 is one of the classical members of the mammalian transient receptor potential (TRP) superfamily of ion channels. TRPC3 is a molecule with intriguing sensory features including the direct recognition of and activation by diacylglycerols (DAG). Although TRPC3 channels are ubiquitously expressed, they
[...] Read more.
TRPC3 is one of the classical members of the mammalian transient receptor potential (TRP) superfamily of ion channels. TRPC3 is a molecule with intriguing sensory features including the direct recognition of and activation by diacylglycerols (DAG). Although TRPC3 channels are ubiquitously expressed, they appear to control functions of the cardiovascular system and the brain in a highly specific manner. Moreover, a role of TRPC3 in immunity, cancer, and tissue remodeling has been proposed, generating much interest in TRPC3 as a target for pharmacological intervention. Advances in the understanding of molecular architecture and structure-function relations of TRPC3 have been the foundations for novel therapeutic approaches, such as photopharmacology and optochemical genetics of TRPC3. This review provides an account of advances in therapeutic targeting of TRPC3 channels. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
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Open AccessReview TRP Channel Involvement in Salivary Glands—Some Good, Some Bad
Received: 8 June 2018 / Revised: 6 July 2018 / Accepted: 8 July 2018 / Published: 11 July 2018
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Abstract
Salivary glands secrete saliva, a mixture of proteins and fluids, which plays an extremely important role in the maintenance of oral health. Loss of salivary secretion causes a dry mouth condition, xerostomia, which has numerous deleterious consequences including opportunistic infections within the oral
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Salivary glands secrete saliva, a mixture of proteins and fluids, which plays an extremely important role in the maintenance of oral health. Loss of salivary secretion causes a dry mouth condition, xerostomia, which has numerous deleterious consequences including opportunistic infections within the oral cavity, difficulties in eating and swallowing food, and problems with speech. Secretion of fluid by salivary glands is stimulated by activation of specific receptors on acinar cell plasma membrane and is mediated by an increase in cytosolic [Ca2+] ([Ca2+]i). The increase in [Ca2+]i regulates a number of ion channels and transporters that are required for establishing an osmotic gradient that drives water flow via aquaporin water channels in the apical membrane. The Store-Operated Ca2+ Entry (SOCE) mechanism, which is regulated in response to depletion of ER-Ca2+, determines the sustained [Ca2+]i increase required for prolonged fluid secretion. Core components of SOCE in salivary gland acinar cells are Orai1 and STIM1. In addition, TRPC1 is a major and non-redundant contributor to SOCE and fluid secretion in salivary gland acinar and ductal cells. Other TRP channels that contribute to salivary flow are TRPC3 and TRPV4, while presence of others, including TRPM8, TRPA1, TRPV1, and TRPV3, have been identified in the gland. Loss of salivary gland function leads to dry mouth conditions, or xerostomia, which is clinically seen in patients who have undergone radiation treatment for head-and-neck cancers, and those with the autoimmune exocrinopathy, Sjögren’s syndrome (pSS). TRPM2 is a unique TRP channel that acts as a sensor for intracellular ROS. We will discuss recent studies reported by us that demonstrate a key role for TRPM2 in radiation-induced salivary gland dysfunction. Further, there is increasing evidence that TRPM2 might be involved in inflammatory processes. These interesting findings point to the possible involvement of TRPM2 in Sjögren’s Syndrome, although further studies will be required to identify the exact role of TRPM2 in this disease. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
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Open AccessReview Ion Channels and Transporters in Inflammation: Special Focus on TRP Channels and TRPC6
Received: 11 June 2018 / Revised: 27 June 2018 / Accepted: 29 June 2018 / Published: 4 July 2018
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Abstract
Allergy and autoimmune diseases are characterised by a multifactorial pathogenic background. Several genes involved in the control of innate and adaptive immunity have been associated with diseases and variably combine with each other as well as with environmental factors and epigenetic processes to
[...] Read more.
Allergy and autoimmune diseases are characterised by a multifactorial pathogenic background. Several genes involved in the control of innate and adaptive immunity have been associated with diseases and variably combine with each other as well as with environmental factors and epigenetic processes to shape the characteristics of individual manifestations. Systemic or local perturbations in salt/water balance and in ion exchanges between the intra- and extracellular spaces or among tissues play a role. In this field, usually referred to as elementary immunology, novel evidence has been recently acquired on the role of members of the transient potential receptor (TRP) channel family in several cellular mechanisms of potential significance for the pathophysiology of the immune response. TRP canonical channel 6 (TRPC6) is emerging as a functional element for the control of calcium currents in immune-committed cells and target tissues. In fact, TRPC6 influences leukocytes’ tasks such as transendothelial migration, chemotaxis, phagocytosis and cytokine release. TRPC6 also modulates the sensitivity of immune cells to apoptosis and influences tissue susceptibility to ischemia-reperfusion injury and excitotoxicity. Here, we provide a view of the interactions between ion exchanges and inflammation with a focus on the pathogenesis of immune-mediated diseases and potential future therapeutic implications. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
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Open AccessReview Role of the TRPM4 Channel in Cardiovascular Physiology and Pathophysiology
Received: 11 May 2018 / Revised: 11 June 2018 / Accepted: 14 June 2018 / Published: 15 June 2018
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Abstract
The transient receptor potential cation channel subfamily M member 4 (TRPM4) channel influences calcium homeostasis during many physiological activities such as insulin secretion, immune response, respiratory reaction, and cerebral vasoconstriction. This calcium-activated, monovalent, selective cation channel also plays a key role in cardiovascular
[...] Read more.
The transient receptor potential cation channel subfamily M member 4 (TRPM4) channel influences calcium homeostasis during many physiological activities such as insulin secretion, immune response, respiratory reaction, and cerebral vasoconstriction. This calcium-activated, monovalent, selective cation channel also plays a key role in cardiovascular pathophysiology; for example, a mutation in the TRPM4 channel leads to cardiac conduction disease. Recently, it has been suggested that the TRPM4 channel is also involved in the development of cardiac ischemia-reperfusion injury, which causes myocardial infarction. In the present review, we discuss the physiological function of the TRPM4 channel, and assess its role in cardiovascular pathophysiology. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
Open AccessFeature PaperReview Remarkable Progress with Small-Molecule Modulation of TRPC1/4/5 Channels: Implications for Understanding the Channels in Health and Disease
Received: 27 April 2018 / Revised: 21 May 2018 / Accepted: 23 May 2018 / Published: 1 June 2018
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Abstract
Proteins of the TRPC family can form many homo- and heterotetrameric cation channels permeable to Na+, K+ and Ca2+. In this review, we focus on channels formed by the isoforms TRPC1, TRPC4 and TRPC5. We review evidence for
[...] Read more.
Proteins of the TRPC family can form many homo- and heterotetrameric cation channels permeable to Na+, K+ and Ca2+. In this review, we focus on channels formed by the isoforms TRPC1, TRPC4 and TRPC5. We review evidence for the formation of different TRPC1/4/5 tetramers, give an overview of recently developed small-molecule TRPC1/4/5 activators and inhibitors, highlight examples of biological roles of TRPC1/4/5 channels in different tissues and pathologies, and discuss how high-quality chemical probes of TRPC1/4/5 modulators can be used to understand the involvement of TRPC1/4/5 channels in physiological and pathophysiological processes. Full article
(This article belongs to the Special Issue TRP Channels in Health and Disease)
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Graphical abstract

Planned Papers

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.

Author: Indu S. Ambudkar
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.
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