Dr. Daniel Koch

Principal Investigator
Cardiac & Cellular Dynamics, Institute of Cardiovascular Sciences

Research Focus

We study how the timing and temporal patterns of molecular signals—like adrenaline or growth factors—shape the behaviour of heart cells and other cell types, influencing processes such as growth, differentiation, and contraction during the heartbeat. Disruptions of these signalling processes can lead to heart rhythm disorders, scarring (fibrosis), and heart failure. Our goal is to understand how the dynamic nature of these signals (e.g., gradual, sudden, or periodic) affects cellular responses.

Why is this work important?

Most of what we know about how heart cells respond to drugs or signals such as (nor-)adrenaline comes from experiments using constant stimuli. But in the body, signals are always changing—hormones like adrenaline fluctuate with physical activity or stress, and cells must adapt to these dynamic environments. By studying these processes, we aim to uncover new ways to design therapies that modulate signal dynamics rather than just targeting new molecules.

What techniques and equipment are used in this laboratory?

We are an interdisciplinary group bridging approaches from biology, physics, and medicine:

Microfluidic cell culture (“heart-on-a-chip”) to mimic dynamic environments.
Live-cell imaging (e.g., calcium, FRET/KTR biosensors) to track cellular responses in real-time.
Molecular/cellular biology approaches (RT-qPCR, immunofluorescence, Western blotting).
Mathematical modelling, dynamical systems approaches (e.g., bifurcation analysis) and data analysis (especially time-series) to decode complex cellular behaviours.

About Dr. Daniel Koch

Dr. Daniel Koch is an assistant professor in the Department of Pharmacology and Therapeutics at the University of Manitoba, a principal investigator at the St. Boniface Hospital Albrechtsen Research Centre and a member of the Maud Menten Institute.

Following studies in philosophy and medicine, Dr. Koch completed a Master’s degree in Cardiovascular Sciences and a PhD in Cell Biology at King’s College London, where he developed a strong interest in cardiac cell biology. To better address the inherent complexity of living systems, he was supported by a fellowship from the European Molecular Biology Organization (EMBO) to pursue postdoctoral training in dynamical systems theory at the Max Planck Institute for Neurobiology of Behaviour in Bonn, Germany.

Dr. Koch’s research aims to understand how cells process and actively contribute to the complex information in their environment and how disruptions of these processes contribute to disease, particularly in the heart. His highly interdisciplinary approach has contributed to new insights into signalling mechanisms in the heart and beyond. A central emphasis of his work is on biological behaviour over time rather than static states, providing conceptual frameworks for understanding living systems in continuously changing environments.

For more information, please contact:

Daniel Koch, M.D. Ph.D.
Principal Investigator
R3042- 351 Tache Avenue
St. Boniface Hospital Research
Winnipeg, Manitoba R2H 2A6
(204) 235-3387, (204) 235-3386

For prospective students/post-docs:

Thank you very much for your interest in our research!

We are always looking for motivated PhD students, graduate students or post-docs. Feel free to submit your application to Dr. Daniel Koch at any time. However, please note the following guidelines for applying: Your application should include a cover letter, a curriculum vitae (including your GPA), letters of reference (if possible) and supplementary data (e.g. your publications, relevant certificates, etc.). The cover letter should state why you want to work in our group (What are your expectations? What would you like to learn?) and why you think you’d be a good fit by addressing your experience in the lab or with theory/computational techniques (if applicable). Unfortunately, we cannot consider applications that appear to be mass-emails and do not follow these guidelines.

Cardiac cells in dynamic environments

The majority of our knowledge about how cardiac and other cells respond to stimuli within the tissue or drugs is derived from experiments based on static stimuli. However, we know that the signals and stimuli our cells receive in vivo are constantly changing over time, for example due to pulsatile release of hormones or changing physical and emotional challenges leading to dynamic changes in neuro-humoral signals such as (nor-)adrenaline in our blood and tissues. The stimulus dynamics – for example, whether a stimulus is released gradually, suddenly or periodically – plays a crucial role in how our cells respond to such stimuli but have not been studied systematically in cardiac cells. A major focus of our group is thus to study cardiac cells such as cardiomyocytes and cardiac fibroblast in dynamically changing environments in which the concentration of extracellular signals (growth factors, catecholamines, cytokines) changes over time to see how their phenotype depends on the temporal characteristics of the stimuli, not only on the molecular identity. Using an interdisciplinary approach, we explore both normal cellular physiology and pathophysiology such as cellular cardiac remodeling during myocardial infarction or heart failure and cardiac arrhythmias to understand how this crucial aspect of in vivo physiology contributes to disease development.

Understanding how cells process time-varying information

While the question of how cells process dynamic signals has begun to receive increasing attention in areas such as immunology, neuroscience and cancer research, most studies focus on a single time-varying input at a time. In living tissues, however, cells receive myriads of stimuli that change over time. Studied in isolation, many of these signals even lead to opposed and conflicting responses. Thus, cells need to be able to integrate multiple pieces of time-varying information simultaneously while at the same time resolving conflicting information in a robust and flexible way to determine their response and phenotype. How cells achieve this by using their intra- and extracellular signaling mechanisms is a fundamental but unresolved issue that touches upon many fascinating questions: How do cells resolve conflicting information? Do cells direct their “attention” to specific inputs depending on context? What is the role of cell-cell communication in this process?

And what is the dynamical basis of processing multi-modal information in intracellular signaling networks?

We aim to answer these fundamental questions using a combination of experimental and mathematical approaches along with ideas from theoretical neuroscience and philosophy with the goal to provide new concepts and approaches for studying and understanding cellular information processing.

Transient dynamics and non-autonomous systems

Formally, the phenotypic responses of our cells are often conceptualized as distinct steady states (or, more generally, what is called an “attractor” in dynamical systems) whose selection is governed by the incoming stimuli a cell receives. However, these often do not provide the necessary flexibility for cells to respond to dynamic stimuli. For this reason, we believe that transient dynamics (dynamics away from steady states or attractors) are required to understand the adaptive nature of cellular signaling responses in dynamic environments. However, identifying origins of transients like ghost attractors, slow-fast dynamics or saddle points in practice remains a challenge for high-dimensional systems. We thus are working on new theoretical frameworks and algorithms to characterize and identify transient dynamics. We further study the role of transient dynamics in non-autonomous systems in which parameters change over time (the formal description of time-varying environments) and its influence on processes such as rate-tipping.

Since transient dynamics and non-autonomous systems are not only found in cell biology but all across disciplines ranging from ecology and climate science to neuroscience, we are also interested in exploring these topics via interdisciplinary collaborations.

Preprints:

D Koch, AP Nandan. Generalized saddle-node ghosts and their composite structures in dynamical systems. 2026. arXiv, 2604.05194.
M Yadav, D Koch, A Koseska. Homeorhetic regulation of cellular phenotype. 2025. bioRxiv, 2025.06. 06.658216.

Peer-reviewed journal articles:

D Koch, A Nandan, G Ramesan, I Tyukin, A Gorban, A Koseska. Ghost channels and ghost cycles guiding long transients in dynamical systems. 2024. Physical Review Letters 133 (4), 047202.
D Koch, A Nandan, G Ramesan, A Koseska. Biological computations: limitations of attractor-based formalisms and the need for transients. 2024. Biochemical and Biophysical Research Communications 720, 150069.
T Kampourakis, S Ponnam, KS Campbell, A Wellette-Hunsucker, D Koch. Cardiac myosin binding protein-C phosphorylation as a function of multiple protein kinase and phosphatase activities. 2024. Nature Communications 15 (1), 5111.
D Koch, A Alexandrovich, F Funk, AL Kho, JP Schmitt, M Gautel. Molecular noise filtering in the β-adrenergic signaling network by phospholamban pentamers. 2021. Cell reports 36 (4),

Full publication list: https://scholar.google.de/citations?hl=de&user=0K1ES48AAAAJ

Awards

EMBO Postdoctoral Fellowship (2022–2024)
Participant of the 72nd Lindau Nobel Laureate Meeting (2023)
King’s Outstanding Thesis Prize, King’s College London (2022)
Outstanding Student Prize in Cardiovascular Sciences programme, King’s College London (2018)
PhD Studentship of the British Heart Foundation (2017–2021)
Studentship by the German National Scholarship Foundation (2013–2016)