Symposia

Preliminary description: This symposium will address the critical role of skeletal muscle in systemic metabolic regulation. Muscle metabolism influences glucose homeostasis, lipid utilization, and energy balance, and is profoundly shaped by both physical activity and dietary intake. Exercise enhances mitochondrial function, insulin sensitivity, and substrate flexibility, while nutrition modulates protein synthesis, recovery, and metabolic adaptation. Cancer may disrupt muscle integrity and insulin sensitivity and may lead to cachexia, but the underlying mechanisms are still unresolved. This symposium will foster interdisciplinary dialogue, highlight translational opportunities, and advance strategies for optimizing muscle as well as whole body metabolism.

Preliminary description: In this symposium we will examine the mechanisms for remodelling of cardiac innervation by which sympathetic overactivation contributes to arrhythmia susceptibility, evaluate emerging therapeutic strategies and bridge the translational gap between preclinical insights and clinical trials.

Preliminary description: Cyclic adenosine monophosphate (cAMP) is a key second messenger present in virtually all cell types, playing particularly critical roles in excitable cells such as neurons and cardiomyocytes. In recent years, the development of genetically encoded cAMP sensors has revealed that cAMP signaling is not uniformly distributed throughout the cell. Instead, distinct nanodomains exist in which cAMP diffusion is locally restricted through compartmentalized production, buffering, and degradation. This spatial organization enables cells to precisely regulate specific signaling events—an aspect that is especially crucial for excitable cell function. Despite these advances, our understanding of how cAMP nanodomains are organized, how they interact, and under which conditions cAMP spreads between them remains incomplete. This symposium will present the latest developments in tools designed to manipulate and monitor cAMP dynamics, along with new insights into cAMP compartmentalization in neurons and cardiomyocytes. The event is co-financed by the Research Unit FOR 5807, and three early-career scientists from the consortium will conclude the session with short flash talks highlighting their most recent findings and experimental strategies.

Preliminary description: Slow cardiac and neuronal pacemaking relies on spontaneous rhythmic activity in the low-frequency range, yet its core ionic mechanisms remain incompletely understood. This symposium will provide an overview of current knowledge and open questions regarding ionic pacemaking mechanisms in the heart and brain. It will highlight the identification of a novel ionic current with distinct functional and pharmacological properties that is essential for slow (1–5 Hz) spontaneous pacemaking in both sinoatrial node cells and midbrain dopamine neurons. This mechanism will be contrasted with ionic processes that support high-frequency (>10 Hz) pacemaking, which are restricted to neurons and involve specialized resurgent currents whose structural basis has recently been elucidated. Finally, recent evidence for plasticity of pacemaker frequency in dopamine neurons following partial lesions will be discussed, illustrating adaptive stabilization of firing patterns in vivo. Overall, the symposium offers a mechanistic update on fundamental principles of pacemaking in heart and brain.

Preliminary description: Physiological regulation emerges from the cell’s ability to communicate effectively within complex tissue environments. G protein-coupled receptors (GPCRs) integrate diverse cellular inputs into context-specific physiological responses. This symposium will highlight recent studies demonstrating how GPCR-mediated signal integration governs key physiological processes. A central aspect to be covered is how selected GPCRs, such as those of the adhesion GPCR family and metabolite-sensing GPCRs, regulate food intake, insulin secretion, energy and glucose homeostasis, or endothelial function. Together, these studies reveal GPCRs as integrative modules that convert cellular signals into defined physiological outputs. By bridging molecular mechanisms with in vivo function, the symposium underscores how GPCRs coordinate intercellular communication to maintain systemic homeostasis and how their dysregulation contributes to disease.

Preliminary description: This symposium examines how hypoxia reshapes iron metabolism and contributes to pulmonary vascular disease across physiological adaptation and pathology. Hypoxia-driven increases in erythropoiesis and hemoglobin synthesis elevate systemic iron demand, which is met through tightly coordinated regulation of intestinal iron absorption, mobilization from iron stores, erythropoietin–erythroferrone signaling, and suppression of hepcidin. Evidence from long-term high-altitude populations and prospective human studies demonstrates that these adaptations can persist chronically, reflecting an integrated response to environmental, genetic, and metabolic cues. Dysregulation of these mechanisms has important clinical consequences, particularly in pulmonary hypertension, where iron deficiency is associated with hypoxia, impaired exercise capacity, and worse outcomes. By integrating experimental and clinical findings, the symposium highlights how altered iron homeostasis and hypoxia-driven vascular remodeling intersect in the development and progression of pulmonary hypertension, providing a unified view of iron–hypoxia interactions across health and disease.

Preliminary description: In addition to its primary function in gas exchange, the lung fulfills a plethora of physiological roles including immunological, hematological, metabolic, endocrine, hemodynamic, and barrier functions that are essential for pulmonary and organismal homeostasis. Accordingly, dysregulation of lung cellular processes and signaling pathways promotes both pulmonary and systemic diseases. The proposed symposium aims to highlight some of these divergent roles: First, it will discuss oxygen sensing in hypoxic pulmonary vasoconstriction as a fundamental regulatory mechanism of gas exchange homeostasis. Next, we will review how dysregulated intercellular crosstalk within the lung drives pulmonary disease in lung fibrosis. We will then expand dysregulated crosstalk to the level of interorgan communication, addressing impaired metabolism as a driver of cardio-pulmonary dysfunction in heart failure. Finally, we will discuss the emerging role of lung organoids for the interrogation of homeostatic and injurious cell circuits in lung health and disease. Overall, the proposed contributions by expert scientists (notably all female and mid-career stage) will provide state-of-the-art insights into hot topics of lung health and disease, ranging from cellular physiology to translational impact.

Preliminary description: The glomerular filtration barrier is a dynamic, multi-layered structure whose dysfunction underlies proteinuria and progressive kidney disease. This symposium will address recent mechanistic insights into the regulation of glomerular permeability, focusing on endothelial specialization, dynamic remodeling of the glomerular basement membrane, and the slit diaphragm as an unconventional cell–cell junction. Novel structural concepts of the blood–urine barrier and emerging models of podocyte-driven control of filtration will be discussed. Together, these contributions aim to refine our understanding of glomerular barrier function and identify new conceptual frameworks relevant to glomerular disease pathogenesis and therapy.

Preliminary description: Minerals such as magnesium, calcium, and phosphate are essential for all forms of life. However, they must also be maintained within narrow physiological limits to avoid a range of pathophysiological consequences. Various organs, including the intestine, kidneys, bone, and endocrine organs, participate in the tight control of these minerals. Dysregulation of mineral balance, either systemic or local, occurs with age and during various diseases, contributing to cardiovascular, metabolic, and bone diseases. Recent advances in this field have revealed new mechanisms of transepithelial mineral transport, new modes of interplay between minerals, new endocrine regulators, novel pathophysiological consequences, and alterations in their control as we age. This symposium will highlight some of these key advances, ranging from cellular mechanisms to whole-organism and integrative physiology in animals and humans.

Preliminary description: In-depth knowledge of the relationship between three-dimensional structure and function of membrane proteins has recently become evident by the emergence of a set of analytical tools such as single particle electron microscopy and molecular dynamics simulations. This insight is not only of interest for the narrow field of protein structure biology but creates new hypotheses regarding their function and paves the way for endeavours into studies of plasma membrane and organellar transport physiology. The field also has a strong pathophysiological relevance and even presents a promise for development of physiologically relevant agonists and antagonists. These developments are strongly represented in the Nordic region and should serve as a huge inspiration broadly among classical physiologists.

Preliminary description: The flow of oxygen and carbon dioxide between the external environment and the metabolizing cells is essential for upholding normal functioning of all animals. These flows can be studied from both macroscopic (e.g. transport in the blood via the circulatory system) and microscopic (e.g. diffusion of gas molecules into cells and mitochondria) perspectives, but with the central requirement that supply has to be matched to demand to maintain homeostasis. Most animals must deal with conditions that challenge the flow of respiratory gases or with changes in the abundance of the respiratory gases themselves. In this symposium, we will explore some of these challenges and the physiological mechanisms adopted by animals to deal with them, from antioxidants of the hyperoxic fish retina to cardiovascular responses of a digesting python. Through presentations of recent and ongoing research, the speakers will also highlight how state-of-the-art technologies are being used by comparative physiologists today, for example spatial transcriptomics, high-resolution respirometry and mass-spectrophotometry.

Preliminary description: Mitochondria are dynamic organelles that are central for the maintenance of cellular energy homeostasis producing ATP via oxidative phosphorylation (OXPHOS). Obesity and type-2 diabetes are intricately linked to impaired mitochondrial functions. In these diseases the peripheral tissues exhibit fragmented mitochondria with impaired OXPHOS capacity, reduced number and mass, enhanced reactive oxygen species (ROS) and the impaired mitochondrial dynamics. Mitochondrial dysfunction is thought to be a consequence of chronic nutrient excess -induced inflammation and oxidative stress. Based on these pathos-mechanisms, targeting mitochondrial function in metabolically active peripheral tissues are considered as a promising treatment approach for these diseases. Lifestyle modifications remain the first line of treatments for metabolic diseases and mitochondrial defects. Among these, exercise, hypoxia and cold exposure are one of the few proven methods for improving mitochondrial functions. In addition, NAD+ restoration therapy is a key treatment approach that involves boosting NAD+ levels. Our symposium will cover the role of mitochondrial signaling in obesity and type-2 diabetes in peripheral tissues. In addition, boosting mitochondrial health by lifestyle changes, and pharmacotherapy to prevent obesity and type-2 diabetes.

Preliminary description: How temperature shapes neural function—from sensory perception to physiological adaptation and neurological vulnerability—remains a fundamental and increasingly urgent question. This symposium examines thermosensory processing across levels of neural organization, from peripheral ion channels that set thermal detection thresholds and guide behavior, to central cortical, thalamic, and hypothalamic circuits that encode temperature and support long-term adaptation. It will highlight mechanisms by which prolonged heat exposure induces plastic changes in neuronal excitability, enabling heat acclimation and tolerance, and will address how thermal stress exacerbates neurological disorders such as epilepsy. By linking molecular, systems, physiological, and clinical perspectives, the symposium provides an integrated view of temperature as a powerful modulator of brain function, with particular relevance in the context of global climate change.

Preliminary description: Mechanosensitive ion channels are membrane proteins that convert physical forces (stretching, shear stress, compression) into electrochemical signals that regulate fundamental cellular processes such as touch sensation, cell volume control, blood pressure regulation, and immune responses. Key families include Piezo and TRP channels whose gain or loss of function are associated with a range of chronic and hereditary diseases, making them important therapeutic targets. The activity of mechanosensitive channels is governed by their physical and biochemical environment. Their dysregulation disturbs ionic homeostasis, particularly Ca2+ signaling, and has been implicated in various disease states, including cardiac arrhythmia and muscular dystrophy. Pharmacological, genetic, and physical tools to control Mechanosensitive ion channel activity are expanding for both basic research and potential clinical applications. This symposium will cover the latest findings on the structure and function of key ion channels involved in force sensing and on how they regulate physiological processes. It will also explore the potential of manipulating mechanosensing for treating human pathologies.

Preliminary description: Sodium–glucose cotransporter 2 (SGLT2) is a key mediator of renal glucose reabsorption in the proximal tubule. In diabetes, enhanced SGLT2 activity contributes to maladaptive renal glucose retention, thereby aggravating hyperglycemia. Pharmacological inhibition of SGLT2 was therefore initially developed as a glucose-lowering strategy. Unexpectedly, large clinical trials subsequently revealed robust renal and cardiovascular benefits that extend beyond glycemic control. Emerging evidence further suggests roles of SGLT2 inhibition in hepatic and neural systems. Despite these advances, the precise mechanisms through which SGLT2 inhibition protects multiple organs remain to be fully elucidated. Accordingly, this symposium is structured around the central question: how targeting renal glucose transport can confer protective effects beyond the kidney. It brings together experimental and clinical perspectives on SGLT2 inhibition in the heart, liver, and brain.

Preliminary description: The immune system is increasingly recognized not as an isolated defense mechanism, but as a dynamic, evolutionarily shaped physiological network that is tightly integrated with multiple organ systems. Rather than acting solely through local immune circuits, immune function is regulated across spatial, temporal, and systemic scales, reflecting pressures imposed by environment, metabolism, reproduction, and neural control. This cross-sectional symposium aims to explore new concepts of immune system physiology, moving beyond classical compartmentalized views of immunity and autoimmunity. Contributions will address how evolutionary forces have shaped immune diversity and regulatory strategies, how immune responses are coordinated at the organismal level, and how central nervous system processes participate in immune regulation, including emerging evidence for long-term neural representations of inflammatory states. Further perspectives will focus on the gut–immune axis as a critical interface between environmental exposure, metabolism, and immune homeostasis, as well as on the unique immunological adaptations required during pregnancy, where tolerance and defense must be precisely balanced.

Preliminary description: Obesity is one of the most complex and pressing challenges in modern medicine, characterized by marked interindividual variability, limited long-term therapeutic success, and profound metabolic consequences. Despite major advances in clinical management and molecular research, fundamental questions remain regarding the mechanisms that govern body weight regulation, treatment response, and disease progression. This cross-sectional symposium aims to integrate clinical perspectives, human genetics, systems physiology, and emerging mechanistic pathways to outline future directions in obesity research. Starting from the clinical realities and therapeutic limitations of obesity treatment, the program will explore why individuals differ so profoundly in susceptibility to weight gain, how central neural circuits integrate peripheral metabolic signals, and which newly identified pathways may serve as targets for next-generation therapies.

Preliminary description: Heart failure remains a major global health burden, with high morbidity and mortality despite substantial therapeutic advances. The disease reflects a complex interplay between molecular mechanisms, clinical heterogeneity, and translational challenges, and while recent progress has reshaped diagnosis and treatment, major gaps remain in understanding patient-specific pathophysiology and implementing innovative therapies. This symposium integrates clinical, translational, and mechanistic perspectives on heart failure, addressing current challenges in patient management, emerging regenerative strategies approaching clinical application, and new insights into disease mechanisms in heart failure with preserved ejection fraction, including the therapeutic potential of targeting myocardial stiffness. Together, the contributions provide an overview of key translational developments that are shaping the future of heart failure therapy.

Preliminary description: This symposium explores the clinical and physiological dimensions of potassium regulation in cardiovascular and renal disease. It will examine the therapeutic potential of a new class of antihypertensive drugs targeting the aldosterone pathway, focusing not only on their blood pressure–lowering and cardiorenal protective effects but also on their impact on potassium balance and the risk of hyperkalemia. At the same time, evidence from randomized trials and systematic reviews indicating cardiovascular benefits of higher dietary potassium intake, as well as data suggesting a protective effect on renal function in early chronic kidney disease, will be critically evaluated in the context of hyperkalemia risk. Integrating these clinical considerations with fundamental insights into the regulation of potassium homeostasis, the symposium will address how potassium levels are maintained within the physiological range in health and disease and how they interact with blood pressure control. Particular emphasis will be placed on whether increasing dietary potassium intake is generally associated with lower blood pressure, independent of dosage and salt intake, providing a cohesive view of potassium regulation across therapeutic, nutritional, and physiological perspectives.