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Unveiling the Complexity of TRPC Channels: From Molecular Mechanisms to Clinical Applications

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 June 2026 | Viewed by 2080

Special Issue Editor

Dr. Oleksandra Tiapko

E-Mail Website
Guest Editor
Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging—Division of Medical Physics and Biophysics, Medical University Graz, 8010 Graz, Austria
Interests: TRPC channels; neurophysiology; photopharmacology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The seven members of the TRPC family are Ca2+-permeable channels found in both excitable and non-excitable cells, indicating their involvement in essential physiological processes. TRPC channels are polymodal and depend on various partners for their activity, including plasma membrane lipids such as diacylglycerol and PIP2, phospholipases, protein kinases, and calmodulin, as well as ion channels like Orai1 and IP3 receptors. Furthermore, emerging evidence links mutations or dysfunctions in TRPC channels to the development of pathologies, for example, cancer and neurodevelopmental disorders, highlighting their potential as targets for pharmacological intervention.

Considering this expanding body of research, we aim to publish a Special Issue of International Journal of Molecular Sciences (IJMS) featuring research and review articles that delve into TRPC–protein/lipid interactions, their role in cellular homeostasis, and novel selective pharmacological strategies for targeting these channels in native tissues. We seek submissions that explore the multifaceted roles of TRPC channels, encompassing their molecular, biochemical, physiological, and genetic dimensions, as well as their impact on the physiology and pathology of tissues where these channels are expressed. We also welcome studies on innovative pharmacological strategies to target TRPC channels in native tissues.

Dr. Oleksandra Tiapko
Guest Editor

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • TRPC channels
  • TRPC–lipid interactions
  • TRPC–protein interactions
  • cellular homeostasis
  • TRPC-dependent disorders
  • (photo)pharmacology
  • TRPC in native tissue

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Published Papers (2 papers)

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35 pages, 6997 KB  
Article
Impact of C-Terminal PKC Phosphorylation on TRPC6 Current Kinetics
by Maximilian Keck, Sebastian Pöll, Hannah Schmelzer, Tabea Kressmann, Christian Hermann, Michael Mederos y Schnitzler and Ursula Storch
Int. J. Mol. Sci. 2025, 26(23), 11482; https://doi.org/10.3390/ijms262311482 - 27 Nov 2025
Viewed by 782
Abstract
Transient receptor potential canonical 6 (TRPC6) channels are promising drug targets for kidney, lung, and neurological diseases, making a detailed understanding of their regulation crucial to developing novel channel modulators with more precise modes of action. TRPC6 channels are commonly accepted as calcium-permeable, [...] Read more.
Transient receptor potential canonical 6 (TRPC6) channels are promising drug targets for kidney, lung, and neurological diseases, making a detailed understanding of their regulation crucial to developing novel channel modulators with more precise modes of action. TRPC6 channels are commonly accepted as calcium-permeable, receptor-operated cation channels activated by diacylglycerol (DAG) downstream of phospholipase C (PLC) signaling. DAG, the endogenous activator of TRPC channels, also activates protein kinase C (PKC), which can phosphorylate TRPC6 and potentially modify its function. This study examined whether five putative PKC phosphorylation sites located in the C-terminus of TRPC6 affect channel gating. Using whole-cell patch-clamp recordings and utilizing photopharmacology with photoswitchable TRPC6 activators (OptoBI-1 and OptoDArG), we analyzed the activation, inactivation, and deactivation kinetics. Pharmacological modulation of PKC activity and strategic mutation of the phosphorylation sites—either to prevent or mimic phosphorylation—altered the current kinetics as well as the normalized slope conductances that were used to quantify differences in the curve progression of current–voltage relations, even when maximally induced current density amplitudes were unchanged. Our findings reveal activator-specific differences in TRPC6 current kinetics associated with C-terminal amino acid exchanges and PKC-dependent signaling, suggesting that phosphorylation-related mechanisms may fine-tune channel activity. Full article
(This article belongs to the Special Issue Unveiling the Complexity of TRPC Channels: From Molecular Mechanisms to Clinical Applications)
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Review

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20 pages, 370 KB  
Review
TRPC Channels as Mediators of Hypoxia-Induced Pulmonary Hypertension in Obstructive Sleep Apnea
by Yolima P. Torres, Andrés Felipe Aristizábal-Pachón and Liliana Otero
Int. J. Mol. Sci. 2026, 27(4), 1861; https://doi.org/10.3390/ijms27041861 - 15 Feb 2026
Viewed by 821
Abstract
Pulmonary hypertension (PH) is a progressive disorder characterized by elevated pulmonary arterial pressure and the extensive remodeling of pulmonary vasculature. Chronic intermittent hypoxia (CIH), a hallmark of obstructive sleep apnea (OSA), is a well-established contributor to the pathogenesis of PH. OSA is defined [...] Read more.
Pulmonary hypertension (PH) is a progressive disorder characterized by elevated pulmonary arterial pressure and the extensive remodeling of pulmonary vasculature. Chronic intermittent hypoxia (CIH), a hallmark of obstructive sleep apnea (OSA), is a well-established contributor to the pathogenesis of PH. OSA is defined by repetitive episodes of upper airway obstruction during sleep, leading to cycles of hypoxia and reoxygenation that trigger a cascade of deleterious events including oxidative stress, inflammation, endothelial dysfunction, and vascular remodeling. Growing evidence underscores the critical role of transient receptor potential canonical (TRPC) channels in mediating hypoxia-induced vascular alterations that contribute to the development of PH. TRPC channels are non-selective cation channels that regulate calcium influx in response to mechanical stimuli, pro-inflammatory cytokines, oxidative stress, and hypoxia. These channels are expressed in both pulmonary arterial smooth muscle cells (PASMCs) and pulmonary artery endothelial cells (PAECs), where they modulate key processes such as proliferation, migration, apoptosis, endothelial permeability, and vasoconstriction. Under hypoxic conditions, the upregulation of TRPC1, TRPC3, TRPC4, and TRPC6 has been implicated in dysregulation of calcium homeostasis and activation of pathological signaling pathways that contribute to increased pulmonary arterial pressure. In this review, we propose that upregulation and functional modulation of TRPC channels under CIH represents a central pathogenic mechanism linking OSA to PH. We hypothesize that TRPC1, TRPC3, TRPC4, and TRPC6 act as critical molecular effectors mediating hypoxia-driven calcium influx and downstream signaling pathways that lead to pulmonary vascular remodeling, endothelial dysfunction, and increased pulmonary arterial pressure. This framework allows us to integrate mechanistic insights from molecular, cellular, and translational studies, and to evaluate the therapeutic potential of targeting TRPC channels in OSA-associated PH. Full article
(This article belongs to the Special Issue Unveiling the Complexity of TRPC Channels: From Molecular Mechanisms to Clinical Applications)
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