Celebrating Physiology in Northern Ireland, June 2026

Belfast’s Professors of Physiology: A Historical Overview

The Chair in Physiology in Belfast was inexorably linked to the training of medical students. The first professor was James Drummond who was appointed to a joint chair in Anatomy and Physiology (and later also Botany!) in 1819. Medical teaching in Belfast predated foundation of a formal medical school, so Drummond’s appointment was in a school, Belfast Academical Institution, which still operates today. Drummond then played a key role in founding the Medical School in 1835 and continued until retirement in 1849, when the school was integrated into the newly opened Queen’s College Belfast. Hugh Carlile was appointed Professor of Anatomy and Physiology in the new school and continued until 1860, when Peter Redfern took over. Like his predecessors, Redfern was more of an anatomist than physiologist. He produced most of his research output on cartilage in his previous post in Aberdeen. Apparently, when he came to Belfast his teaching duties, for which he was widely revered, took over. Throughout the middle of the 19^th century, Physiology gradually began to acquire its own identity, so, with the foundation of the Physiological Society in 1976, it was natural to split Redfern’s post when he retired in 1893. Hence, William Henry Thompson became the first Dunville Professor of Physiology, which takes its name from an endowment from the wealthy Dunville family of distillers in Belfast. Thompson was a man of great talent and wide research interests which included studying the effects of ‘Peptone’ when injected into the circulation, lesions of the temporal cortex, the effect atropine and morphine on urine output and the metabolism of arginine. In 1902, Thompson moved on to Trinity College Dublin and was replaced by Thomas Milroy. Milroy was a quiet man, but a productive researcher, again in diverse areas. He and his brother John, who became Professor of Biochemistry, are commemorated by the Milroy Medal, awarded annually to the top Queen’s medical student in Physiology and Biochemistry. Henry Barcroft became the next Dunville Professor in 1935 and with him began a golden age for Physiology in Queen’s. He studied human blood flow by venous occlusion plethysmography and this continued with David Greenfield, the next Dunville Professor, when Barcroft left for Thomas’s Hospital Medical School in 1948. Under Greenfield, Physiology in Queen’s reached its zenith with many of his mentees going on to high profile posts across the world. Examples include ‘Darty’ Glover (Dean of Medicine in Sydney), Bob Whelan (Vice-Chancellor of the University of Western Australia and, later, of the University of Liverpool) John Shepherd (chairman of the Board of Development at the Mayo Clinic) and Ian Roddie, who became the next Dunville Professor in 1964. Greenfield himself went on to found the medical school in the University of Nottingham. Under Ian Roddie’s stewardship, a field of research in lymphatic physiology developed in Queen’s, with two of his co-workers becoming, in turn, the most recent Dunville Professors, namely Noel McHale and Graham McGeown, both of whom also served their time on the Committee of the Physiological Society.

‘Exercise Physiology Research at Ulster University: Highlights and Future Directions

Exercise is a well-known stressor that disrupts the body’s normal physiological state, with the physiology of exercise further concerned with how the body functions and responds to the dynamic challenge of skeletal muscle contractions. Ulster University’s Sport and Exercise Sciences Research Institute (SESRI) was established in 2002, and since then, Exercise Physiology research has become a cornerstone of the Institute’s research outputs. SESRI’s work, to date, has demonstrated how during exercise, cells, tissues and organ systems are affected, initiating diverse physiological responses such as altered gene expression, enhanced vascular function, changes to free radical metabolism, and DNA damage that can all be applied in different contexts. Thus, exercise is a remarkable lens through which normal bodily function can be explored. This presentation will summarise SESRI’s research demonstrating the molecular, cellular and systemic responses to exercise (both acutely and following training) that underpin adaptations, which can be harnessed to improve training responsiveness, performance and/or health parameters. Specifically, the presentation will focus on research that has sought to understand how exercise of different types, intensities, and durations can elicit different physiological responses, and the mechanisms through which these effects manifest through oxidative stress and inflammatory related pathways. We have also been concerned how supplements such as a broad range of antioxidants have the potential to modify responses to exercise stimuli, and how the physiological compensations to exercise may be affected by certain environmental factors such as hypoxia. Collectively, our data have been used in basic, applied, translational and clinical contexts such as for the prevention and treatment of chronic diseases. This talk will highlight some of our emerging and future research directions including how circadian principles may be applied to exercise prescription for both health and performance outcomes.

Teaching Physiology in the Global Village.

Historically, physiology teaching was content-heavy, dominated by didactic lectures and rote learning. I will discuss how much modern physiology education has departed from this practice.

It is a truth universally acknowledged, that physiology is the cornerstone of medicine, but a notoriously difficult subject to learn. Therefore, a physiology student must be in want of an exceptional teacher. In the past, knowledge was transmitted passively from expert to learner (the so-called “Sage on the Stage”; King, 1993). There was limited consideration of how students learn. A modern, student-centred approach facilitates active, inquiry-based learning (the “Guide on the Side”; King, 1993), including case-based learning, which is integrated into the medical curriculum at Queen’s University Belfast (QUB). Research shows that active learning improves conceptual understanding and enhances student engagement (Freeman et al., 2014). Alongside, formative feedback and authentic assessments that emphasise reasoning, integration, and application of knowledge rather than memorisation, train students in key transferable skills required for future employment as part of the global workforce.

The modern physiology educator is increasingly a scholarly teacher. QUB researchers are using evidence to guide practice while preparing learners to apply physiological understanding responsibly across diverse health, environmental, and sociocultural contexts. For example, McGahon et al., (2026) integrated the UN Sustainable Development Goals (SDGs) into physiology education, highlighting how a knowledge of physiology is relevant to a student body who care deeply about the world we live in and its people. This group’s work contextualises physiology learning to the societal and global issues of today, including global warming, health inequalities, and aging populations. Roe et al., (2024) describes an innovative arts-meets-science approach to teach hypofertility and behavioural skills (for example, respect, empathy, compassion, and interpersonal skills) to medical students, using final year Drama students as simulated patients. The research found that realistic simulations of doctor-patient interactions felt authentic and emphasised the importance of physiology to patient care, while also embedding “human factors” skills that enhance the overall educational experience.

Digital technologies, the use of which rapidly increased during and after the COVID-19 pandemic, have further reshaped physiology education into a “global village”. Collaboration between institutions is easier, and shared curricula and co‑teaching can be supported across borders and time zones. Virtual physiology laboratories and simulations have become more widespread, particularly in regions where laboratory infrastructure, funding and/or time is limited. More recently, learning analytics and artificial intelligence offer opportunities for a personalised learning experience no matter where you learn. The increased volume and velocity of information now enables rapid, worldwide interaction which the education community is harnessing. However, this hyper-connection comes not without its challenges. Our unpublished research suggests that educators struggle with the “always on” nature of work post-COVID-19 and the blurring of professional boundaries.

In summary, the physiology educators of 2026 must prepare students for a rapidly changing world where critical thinking and problem-solving are essential to the application of physiology to current and future global challenges.

Physiology approaches in Cancer Research: Unlocking New Targets to Improve Therapy

At Queen’s University Belfast, physiology education and research has built a legacy of discovery science with translation in health and disease. Application of physiology research approaches to cancer research has identified novel targets with the potential to enhance therapy and improve outcomes. This presentation will highlight two of our research programmes: ‘radiotherapy-induced bladder dysfunction’ and ‘ion channels and cancer’.

Radiotherapy aims to maximise tumour control and minimise adverse effects on neighbouring normal tissue. Despite innovations that more precisely deliver radiation to tumours, many patients experience side-effects from normal tissue toxicity. In pelvic cancers, radiotherapy can evoke acute radiation cystitis and bladder dysfunction which often resolves over time. Late effects are less common, occurring months to years post-radiotherapy, but cause significant and irreversible bladder dysfunction. Investigation of bladder physiology after irradiation is uncovering the underlying pathophysiological mechanisms. CT image-guided radiation of mice bladders recapitulated the clinical context where around 50% of mice exhibited altered voiding patterns with frequent, small volume voids. Interestingly, contractility of bladder tissue strips was changed after irradiation, whether or not voiding patterns were changed. Neurogenic-contractions were smaller in the acute phase, 2 weeks post-radiation and while they increased over subsequent months, did not fully resolve. Impaired contractility was not explained by aberrant voltage-gated Ca²⁺-activity as depolarization-mediated contractions were unaffected by irradiation. Muscarinic-contractions were also unaffected; therefore, pre-synaptic mechanisms may be radiation-sensitive and further work is needed to better understand this (1).

Ion channels are linked with many cancer hallmarks, with altered mRNA and protein expression of diverse ion channels across many cancers vs. normal tissue commonly reported (2). Interestingly, further changes are detected following cancer treatment. Specialist physiology techniques are necessary to reveal whether these changes translate to aberrant ion channel signalling which contributes to cancer growth, treatment resistance and metastasis. Such work can indicate whether ion channel drugs, used in the clinical management of other conditions, could have therapeutic benefit for cancer.

We, and others, have shown that upregulation of the L-type Ca²⁺-channel, Ca_V1.3, encoded by CACNA1D, is common in prostate cancer, tracking with Gleason grade and metastasis status. Hormone therapy conditions, via androgen deprivation or androgen receptor inhibition, further upregulates CACNA1D expression, sustains Ca_V1.3 overexpression and may enhance localisation at the plasma membrane. Of note, Ca_V1.3 ion channel activity could only be detected during hormone therapy conditions with patch-clamp electrophysiology or Ca²⁺-imaging (3). This suggests that Ca_V1.3 activity, emerging during hormone therapy, when proliferative capacity is reduced may facilitate adaptation and survival of treatment-resistant cells that eventually drive recurrence. It remains to be seen whether repurposing calcium channel blockers could be of therapeutic benefit during hormone therapy.

The presentation will share how using physiology lenses in cancer research can foster collaborative, interdisciplinary working that may ultimately improve patient outcomes and quality of life.

Forty years in Physiology goes by in a flash!

Nearly four decades have passed since I first walked through the doors of Queen’s University Belfast in September 1986 to study Physiology as an undergraduate. Since then I’ve been fortunate to build a career alongside outstanding colleagues, united by a shared curiosity about how smooth muscle generates and shapes electrical signals to drive physiological function.

A central theme of the research in our Smooth Muscle Research Centre has been the characterization of ion channelsand their role in regulating the electrical and mechanical activity of lymphatic^1-4, lower urinary tract^5-15and airway smooth muscles^16-19. Earlier in my career, this led to a significant technical and scientific challenge: the study of lymphatic smooth muscle. At the time, few scientists had successfully recorded electrical activity from freshly isolated lymphatic smooth muscle cells. Nevertheless, we established reliable cell isolation procedures and managed to utilise patch clamping to characterise the major ionic currents in lymphatic smooth muscle^1-4 and lay the foundations for future work on how electrical activity governed lymphatic contractility.

Around the same time, we demonstrated for the first time that interstitial cells of Cajal (ICC), well established as pacemaker cells in the gastrointestinal tract, were also present in non-gastrointestinal smooth muscles^6-10. This finding expanded the conceptual framework of how smooth muscle contractile activity was generated and coordinated. Subsequent work, supported by NIH funding, explored the electrophysiological properties of these cells and their modulation by neurotransmitters, helping to establish ICC and related cell types as key intermediaries in smooth muscle signalling across multiple organ systems.

We were also fortunate to be actively engaged in translational collaborations with industry. In the early 2000s, in partnership with Andor Technology, we were glad to help in the development of electron multiplying CCD (EMCCD) cameras for biological imaging^20-22. Originally designed for astronomy, these sensors transformed the ability to detect low Ca²⁺ signals in single cells and tissues, overcoming limitations of earlier imaging systems. Since their commercial introduction in 2003, EMCCD technology quickly became a cornerstone of live-cell imaging, illustrating the impact of cross-disciplinary innovation.

More recently our work has focused on the development of novel ion channel modulators and how they interact with their targets at the molecular level. Through the synthesis and characterization of a novel family of GoSlo-SR compounds we have generated potent ion channel modulators^23-25, determined their molecular mechanism of action²⁶ and patented the most promising structures²⁷.

Complementing this in 2020, we identified the LINGO family of proteins as previously unrecognized regulatory subunits of BK channels^28-31. Given the upregulation of LINGO proteins in Parkinson’s disease²⁸, we have proposed a mechanistic link between LINGO-associated BK channel dysfunction and the emergence of Parkinsonian tremor, opening new avenues for therapeutic intervention. In this invited talk, I’ll focus on some of our more recent research in which we’ve examined the molecular mechanisms underlying BK channel modulation by these novel regulatory LINGO subunits.

The impact of misalignment with the external light-cycle on diabetic retinopathy

Circadian disruption can be experienced when one lives in a misalignment of their internal clocks with the environmental light cycles. In this study, we investigated whether a form of circadian disruption experienced by extreme chronotypes impacts the progression of diabetic retinopathy.

Ins2 Akita, hyperglycemic, male mice and healthy controls, at two months of age, were housed for 4 months in a forced desynchrony conditions within the limits of entrainment with light cycles (T22.5 and T27 cycles) that resemble circadian disruption of late and early extreme chronotypes correspondingly. Eye disease endpoints were assessed with in vivo retinal imaging (fundus imaging, OCT), ex-vivo immunohistological approaches for acellular capillaries and vascular morphology, and retina tissue was used for mRNA sequencing. Two Way ANOVA (diabetes, chronotype) was used to identify statistically significance (p<0.05)

Retinal thickness was significantly reduced in diabetes by 7% compared to controls and was further reduced by another 7% in both forced desynchrony conditions. The number of acellular capillaries in diabetes was increased by 48% in the diabetic mice undergoing forced desynchrony with effects on the intermediate and deeper vascular layers, where significantly reduced vessel area, vessel length and increased E-lacunarity. The mRNA sequence of the retina confirmed that forced misalignment in diabetes impacted the retina vasculature more than in control. Genes related to one carbon metabolism were among the top genes mostly affected by forced misalignment in diabetes, while a more inflammatory pathway activation was also observed. We further validated a particular target with immunofluorescence, its regulation by the clock and its effect on ednothelial cell physiology in vitro.

Overall, a misaligned light schedule to the internal clock that simulates the social jet lag experienced by extreme chronotypes leads to an acceleration of the retinal structure and microvascular dysfunction observed in diabetes. The effects are manifested due to circadian clock disruption and particularly affect the stress responses to the misalinged light. Circadian disruption could therefore be a modifiable risk factor for prevention of diabetic retinopathy.

Busting the Myth of 70Kg Man Through Participation in an Anthropomorphic Data Practical

Historically the discipline of Physiology has had 70Kg “Physiologic” man as a foundational reference model representing an assumed average individual from which “normal” values could be derived (Phillips, 2023). While this may prove useful, the limitations of the concept of “average” man have become more apparent recently, especially in the context of medical education and research with a diverse and global cohort of students, subjects and patients. Students who do not see themselves in the curriculum do not learn as effectively, (Ahmet, 2010; Koens et al., 2005) and the reliance on the male standard promotes a gendered stereotype of physiologic knowledge (Cheng & Yang, 2015).

To challenge the “Physiologic Man” model, we have designed a “Busting the Myth of 70Kg Man” practical to illustrate the wide variability in physiologic data across populations and challenge the myth that a “typical” human exists. Students measure height, weight, body fat percentage, stretch, jump and endurance performance in a practical class. As well as gaining experience in measuring human variables, participants get the opportunity to interpret data and draw inferences from raw numbers. That way, the skills of interpolation are inculcated as well as physiologic principles. The remit of the practical also includes issues around professionalism, informed (and immediately withdrawable) consent, anonymising data, bodily autonomy of volunteers, and awareness that the measurement of some variables (weight and body fat percentage) can be triggering.

After gaining ethics committee approval, a mixed methods approach was used combining both electronic survey data and focus group discussions from 2^nd Year Medicine (Exercise and Applied Physiology Student Selected Component (n=14) and Science (Human Biology Degree Programme (n=4) students. The survey assessed students’ knowledge of and opinions on the importance of inclusion in the physiology curriculum and their lived experience of completing the practical (both as investigator and subject). Changes in attitudes on undertaking the practical were evaluated with pre- and post- practical Likert questionnaires that calculated responses to statements about the classes from 1 (Strongly disagree) to 5 (Strongly agree). Differences between groups were tested for significance using a Wilcoxon signed rank test. In addition, open questions supplemented the Likert semi-quantitative data, allowing students to express opinions and relate experiences. Focus groups were also conducted to give further opportunity to students to relay their experiences. Thematic analysis of the focus group transcripts and answers to open questions allowed us to develop themes using the framework of Braun and Clarke (2006).

Students disagreed with the contention that 70Kg man was an appropriate reference point for teaching physiologic norms (Mean (±SEM) Likert scores: Female=1.7±0.83, Male=2.2±0.4, Non Binary (NB) =1±0), with slightly more men than women thinking the model was appropriate. Similarly, males felt themselves better represented in the physiology curriculum ((Mean (±SEM) Likert scores: Male=3.8±1.2, Female=2.1±0.4, NB=2±0). Students found the experience of the practical profoundly affecting, gaining a regard for the importance of communication, emotional safety and the primacy of consent when gathering these data. Students especially stressed the importance of the instructor’s language and the tone of respect thus set.

Investigating the Mechanisms Underlying Cardiomyopathy in Diabetes Mellitus Using iPS-Derived Cardiomyocytes

Introduction

Type II diabetes mellitus is a rapidly growing worldwide health challenge. Diabetic cardiomyopathy is a heart muscle disease characterised by progressive contractile dysfunction independent of coronary artery disease or hypertension. It is driven by metabolic dysfunction, oxidative stress, calcium mishandling and mitochondrial impairment. Classical disease models are limited in their ability to replicate human-specific disease mechanisms. Therefore, we used induced pluripotent stem cell-derived cardiomyocytes (iPS-CMs) to provide a strong patient-specific model for investigating cellular and molecular changes in diabetic cardiomyopathy, as they retain donor-specific metabolic and epigenetic characteristics.

Methods

iPSCs generated from three diabetic and three non-diabetic donors were differentiated into cardiomyocytes through temporal modulation of Wnt/β-catenin signalling. The iPSC-derived cardiac cultures contained a heterogeneous population of cardiomyocytes (CMs) and cardiac fibroblasts (CFs), better recapitulating the native myocardial microenvironment. Molecular and functional comparisons were performed using immunofluorescence, RT-qPCR, Western blotting, RNA sequencing, and live-cell fluorescence assays. Functional phenotyping included measurements of mitochondrial reactive oxygen species (ROS), apoptosis, and Ca²⁺ dynamics.

Results

Diabetic iPSC-CMs exhibited increased oxidative stress, elevated apoptosis, and a marked increase in hypertrophic markers associated with cardiac stress, including ANP, BNP, GATA4, and ANKRD1, as well as fibrotic markers including TGFB1, CTGF, FN1, POSTN, COL1A1, and COL3A1. Flow cytometry revealed increased forward scatter (FSC) in diabetic TNNT2+, confirming a hypertrophic phenotype. Furthermore, higher FSC-A of vimentin+ and PDGFRα+ populations, along with a higher proportion of α-SMA-positive cells, indicated increased cardiac fibroblast proliferation and myofibroblast activation. Calcium imaging revealed profound defects during excitation–contraction coupling, characterised by elevated baseline cytosolic Ca²⁺, reduced sarcoplasmic reticulum Ca²⁺ stores, and delayed Ca²⁺ reuptake, consistent with impaired diastolic relaxation.

RNA sequencing of iPSC-CMs from three donors per group identified 1,412 differentially expressed genes. Pathway enrichment and gene ontology analyses revealed significant upregulation of gene networks related to cardiac hypertrophy, fibrosis, ECM remodelling, and ion channel regulation in diabetic iPS-CMs. The WNT/β-catenin and TGF-β signalling pathways were prominently enriched, both of which serve as key drivers of maladaptive hypertrophic and fibrotic remodelling in the diabetic cardiac phenotype.

Pharmacological inhibition of Wnt signalling partially rescued the diabetic phenotype, reducing oxidative stress and improving calcium handling in contractile cardiomyocytes. attenuating TGFβ signalling, as demonstrated by reduced SMAD2/3 activation and decreased secretion of TGFβ1 and PAI-1, in addition to hypertrophic markers such as secreted ANP.

Conclusion

Collectively, this study shows that donor-specific iPSC-CMs can recapitulate key features of diabetic cardiomyopathy and provides mechanistic insights, linking aberrant signalling pathways to functional impairment. This work highlights the potential of testing donor-specific therapeutic targets and establishes a clinically relevant platform for treating diabetes-associated heart disease.

Modulation of contractions and cytosolic Ca2+ by cAMP and its downstream effector proteins, EPAC and PKA

Penile erection is mediated by relaxation of corpus cavernosum smooth muscle (CCSM), primarily driven by cyclic nucleotide signalling. Current therapies for erectile dysfunction (ED) target the nitric oxide (NO)-cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG) axis, with phosphodiesterase-5 inhibitors (PDE5Is) enhancing cGMP signalling to promote relaxation. However, 30-40% of patients, particularly those with diabetes or vascular disease, respond poorly due to impaired NO bioavailability and reduced cGMP formation, limiting efficacy ^[1].

The parallel cyclic adenosine monophosphate (cAMP) pathway represents an alternative target, traditionally attributed to protein kinase A (PKA)-mediated reductions in intracellular Ca²⁺. Clinically, this is exploited via intracavernosal prostaglandin E1 (PGE1; alprostadil). PKA also modulates ion channels, including K_v7.5 channels, expressed in mouse CCSM cells ^[2]. More recently, exchange protein directly activated by cAMP (EPAC) has emerged as a distinct cAMP effector, inducing smooth muscle relaxation via Rap1/2 signalling, though its role in CCSM remains poorly defined.

Using selective activators of PKA (6-MB) and EPAC (007-AM), we investigated their contributions in mouse CCSM. EPAC-1 expression was confirmed at transcript (RT-PCR, qPCR) and protein levels (immunoreactivity in isolated CCSM cells), with antibody validation in mouse kidney cortex, which highly expresses EPAC-1 ^[3].

In isometric tension studies, CCSM pre-contracted with phenylephrine (PE; 3×10^-7M) exhibited sustained phasic activity. EPAC activation (007-AM, 1×10^-5M) produced modest but significant reductions in contraction frequency (6.87±1.47 min^-1 to 5.17±1.07 min^-1; P=0.0156) and amplitude (0.99±0.16 mN to 0.86±0.16 mN; P=0.0276). Similarly, PKA activation (6-MB, 1×10^-4M) reduced contraction frequency (6.70±0.59 min^-1 to 4.57±0.47 min^-1; P=0.0001). However, co-activation abolished phasic contraction frequency (5.83±0.94 min^-1 to 0.00±0.0 min^-1; P=0.0016) and amplitude (0.87±0.14 mN to 0.00±0.0 mN; P=0.0015).

At the cellular level, PE induced Ca²⁺ oscillations in isolated CCSM cells. 007-AM significantly reduced oscillation frequency (20.0±4.0 min^-1 to 0.5±0.5 min^-1; P=0.0087) at high PE (1×10^-5M), previously identified as membrane potential-independent ^[2]. In contrast, 6-MB had no effect under these conditions (25.7±4.2 min^-1to 25.2±3.5 min^-1; P=0.8560) but abolished oscillations (9.5±0.9 min^-1to 0.0±0.0 min^-1; P=0.0445) at low PE (1×10^-7M), which are membrane potential-sensitive. This effect was prevented (8.0±1.0 min^-1to 15.5±2.1 min^-1; P=0.4896) by the K_v7 blocker XE-991, implicating K_v7 channels in PKA-mediated responses.

Collectively, these data show that EPAC-1 is expressed in CCSM and inhibits Ca²⁺ signalling, potentially via suppression of sarcoplasmic reticulum Ca²⁺ release, while PKA may promote relaxation through K_v7.5 channel activation and membrane hyperpolarisation. Although co-application of 007-AM and 6-MB abolished contractions, the ability of EPAC activation alone to suppress Ca²⁺ oscillations suggests a dominant role for EPAC rather than simple additive effects. Targeting cAMP effectors, particularly EPAC, alone or alongside PKA, may therefore offer a strategy to restore CCSM relaxation in patients unresponsive to PDE5Is.

The Hidden Order Controlling Endothelial Function

The endothelium forms a vast, distributed interface between blood and tissue that continuously integrates mechanical and chemical signals to regulate virtually every cardiovascular function. Endothelial function has traditionally been viewed as arising from a largely uniform population of cells that respond in parallel to external stimuli. Vascular function, it is proposed, reflects the averaged output of equivalent cellular units, with each endothelial cell behaving as a scaled-down representation of the average response of the population. However, this view struggles to explain how coherent vascular responses emerge reliably across space despite pronounced cellular heterogeneity, multiple different simultaneous functional outputs and complex signalling environments. We combine high-resolution calcium imaging with network-based analyses to reveal that endothelial behaviour is governed not by individual cells, but by the structure of their interactions. We show that endothelial signalling forms a highly-organised network characterised by small-world and scale-free properties. Within this architecture, distinct subpopulations of cells play specialised roles. Some act as connectors, linking different groups of cells and integrating signals across the network. Others act as hubs, exerting strong influence within highly coordinated regions. These features enable rapid, robust, and spatially-coordinated signalling to occur. The features also introduce non-linear signalling dynamics, where the relationship between input and output is not proportional but depends on the state of the network. Local changes in activity can be amplified or suppressed through interactions in highly-connected regions. Similar inputs are unaltered in less connected or fragmented areas. As a result, identical stimuli can produce markedly different outcomes depending on how signals are distributed and integrated across the network. This non-linearity gives rise to emergent signalling, where system-level responses arise from the collective interactions of cells rather than from the behaviour of any individual component. Signals are not simply transmitted, but are reshaped, amplified, or dampened by the network through which they propagate. As a result, endothelial responses reflect the organisation of connectivity rather than the properties of individual cells alone. Function, therefore, emerges dynamically from patterns of interaction, enabling coordinated, adaptive and independent multifunctional responses across space. These findings reveal that endothelial behaviour is governed by distributed control arising from local interactions that collectively generate system-level function. Furthermore, they shift the focus from single-cell mechanisms to network architecture as the key determinant of function, stability, and vulnerability in endothelial control. In this framework, there is no central controller; instead, vascular responses arise from a form of collective, network-based intelligence. We propose that the hidden order controlling endothelial function lies in its network architecture, so redefine control as an emergent property of connectivity.

Registration opens	25 February 2026
Abstract submission opens	25 February 2026
Abstract submission closes	25 March 2026
Conference Attendance Award deadline	30 April 2026
Registration deadline	11 June 2026
Meeting date	25 June 2026

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Thursday 25 June 2026

Celebrating Physiology in Northern Ireland

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09:05 SA01 Belfast’s professors of physiology: A historical overview

09:30 SA02 Exercise physiology research at Ulster University: Highlights and future directions

09:55 SA03 Teaching physiology in the global village

11:00 PL03 Establishing equity in medicine admissions

13:00 SA05 Gut peptides in the therapy of obesity and diabetes

13:25 SA06 Physiology approaches in cancer research: Unlocking new targets to improve therapy

13:50 SA07 Forty years in physiology goes by in a flash!

14:15 SA08 The impact of misalignment with the external light-cycle on diabetic retinopathy

15:00 C01 Busting the myth of 70Kg man through participation in an anthropomorphic data practical

15:15 C02 Investigating the mechanisms underlying cardiomyopathy in diabetes mellitus using iPS- derived cardiomyocytes

15:30 C03 Gene therapy-mediated modulation of angiopoietin signalling rescues blood flow changes in the diabetic mouse retina

15:45 C04 Modulation of contractions and cytosolic Ca2+ by cAMP and its downstream effector proteins, EPAC and PKA

16:00 SA09 The hidden order controlling endothelial function

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