TRPC.at doctoral program

This project investigates how the calcium-permeable ion channel TRPC3 regulates neuronal activity in the hippocampus and how disease-associated mutations alter brain function. We aim to uncover how disrupted calcium signaling contributes to neurodevelopmental disorders by combining advanced electrophysiology, calcium imaging, and photopharmacology with patient-derived TRPC3 variants in transduced primary hippocampal cultures. Understanding these mechanisms will provide fundamental insight into ion channel dysfunction in the brain and may identify new targets for therapeutic intervention.

Using biosensors, reporter systems, and advanced microscopy, we will reveal how lysosomes orchestrate mitochondrial responses and iron-dependent cell death, uncovering hidden triggers of ferroptosis with therapeutic potential.

In this project, the PhD-student will work on assessing the role of TRP channels in pulmonary fibrosis, a chronic progressive lung disease. Strategies aimed at modulation of TRP channels will be tested for potential anti-fibrotic effects in vivo, ex vivo and in vitro. This is of special interest as current therapeutics have limited efficacy and novel drugs are urgently needed.

In this exciting project the PhD student will make use of advanced computational methodologies to assess the molecular basis of the pathophysiology of TRPC channels. Starting from the simulation of the dynamics of these channels, the PhD student will establish new descriptors to navigate the functional mutational landscape in TRPC channels. The PhD student will benefit of the experimental know-how within TRPC.at to validate their methodology. The generated information will be used to look for new probes and potential drugs to monitor and modulate the response of these extraordinary channels.

Macrophage-driven inflammation critically shapes lung injury outcomes. We propose that a BK–TRPC ion channel axis controls macrophage calcium signaling and polarization. Dysregulation of this pathway sustains pro-inflammatory responses and tissue damage, while targeted TRPC modulation may restore resolution, offering a novel ion-channel–based therapeutic strategy for inflammatory and fibrotic lung disease.

This PhD project investigates how chronic activation of TRPC3 and TRPC6 channels contributes to pathological cardiac remodeling and heart failure. Focusing on angiotensin II–mediated calcium signaling, it examines how disrupted subcellular calcium homeostasis drives hypertrophic and inflammatory gene programs. Combining molecular, electrophysiological, imaging, and in vivo approaches, the study aims to uncover mechanisms linking TRPC signaling to cardiac dysfunction.

This project investigates how TRPML1 regulates interaction between mitochondria and lysosoms during cancer energy stress, focusing on ion signaling at nanoscale contact sites and dynamic mitochondrial ultrastructure organization. Structured illumination microscopy will connect mitochondrial membrane potential patterns with organelle organization in living cells. The project addresses fundamental mechanisms of organelle communication in cancer.

This project investigates immune cell–specific roles of TRPC3/6 Ca²⁺ channels in psoriasis. Combining genetic mouse lines and a well-established murine model of psoriasis-like skin inflammation, it aims to define how TRPC3/6 regulate immune cell activation and evaluate their therapeutic potential in psoriatic disease.

In this project, the PhD student will investigate the role of TRPC6 channels in eosinophilic airway inflammation, with a particular focus on allergic asthma. Functional and molecular analyses in human eosinophils and murine models will be combined to elucidate TRPC6-dependent signaling pathways and their contribution to disease pathogenesis. The therapeutic potential of targeting TRPC6 will be evaluated using pharmacological modulators and a house dust mite-induced model of allergic lung inflammation, aiming to identify novel strategies for immune modulation in asthma.

This project examines how TRPC1/3/6 ion channels influence calcium dynamics in pulmonary vascular cells, contributing to disease-related remodeling. Integrating photo-pharmacology, advanced imaging, ion-channel physiology, and bioinformatics, we aim to uncover novel strategies to modulate vascular tone. The PhD candidate will train across murine and human systems, bridging basic science and translational medicine.

This project investigates how TRPC5 channels located in extracellular vesicles, contributes to cancer progression and chemoresistance. We will investigate calcium signaling in breast cancer using a vascularized chicken embryo (CAM) model, combining high-resolution fluorescence and Ca²⁺ imaging. Using photopharmacologically tools to manipulate TRPC5, this study will assess how calcium-dependent extracellular vesicle transfer influences gene regulation, tumor remodeling, and chemoresistance development.

This PhD project investigates how age-related alterations in reactive oxygen species (ROS) affect the activity of redox-sensitive TRP ion channels. Using live-cell fluorescence microscopy with organelle-targeted biosensors alongside molecular biology approaches, it will map ROS-TRP interactions and the downstream pathways they engage during aging. Mechanistic findings will be linked to organismal outcomes in C. elegans and then tested for conservation in mammalian cellular aging models.

TRP channels influence the development and excitability of cerebellar Purkinje cells. This project uses a cerebellum-like circuit in the brain of the fruit fly to pinpoint the mechanisms by which TRP channels shape the growth and function of neurons. It combines genetics, in vivo electrophysiology, and two-photon microscopy.

This project investigates how localized, membrane-proximal hydrogen peroxide signals regulate redox-sensitive TRP channels and thereby control neuronal and cardiac excitability. Using patch-clamp electrophysiology combined with light-activated materials to generate precisely timed oxidative stimuli, it quantifies how ROS modulate ion channel gating and action potential dynamics in real time. The aim is to define how oxidative stress is translated into pathological hyperexcitability, contributing to pain sensation and cardiac arrhythmias.

Emerging evidence suggests an important role for cardiac TRP channels in both atrial and ventricular proarrhythmic remodeling. This project employs mechanistic computational models of cardiomyocytes and fibroblasts to better characterize the role of TRP channels in cardiac calcium-dependent signaling pathways and proarrhythmic remodeling, and to identify potential novel therapeutic targets.