Research groups
Websites
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Oxford BHF CRE
Centre of Research Excellence
Collaborators
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Pawel Swietach
Professor of Physiology
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Manuela Zaccolo
Deputy Head of Department
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Heidi de Wet
Associate Professor of Physiology
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Francis Szele
Associate Professor of Developmental Biology
Colleges
Liron Boyman
PhD
Group Leader
- British Heart Foundation Intermediate Basic Science Fellow
- Principal Investigator at Oxford BHF Centre of Research Excellence (CRE)
Molecular Physiology of the Mitochondria
My research centers on the molecular physiology of the mitochondria—the tiny powerhouses within our cells that generate energy, produce heat, and make complex multicellular life possible. While essential for sustaining life, mitochondria also play a central role in the development of a wide array of diseases, including heart disease, neurodegeneration, and cancer.
The identities and properties of mitochondrial ion transport systems and key signaling pathways are under intense investigation by a rapidly expanding field of research. These high-profile molecular discoveries reflect the tremendous interest in the energy producing organelle and the growing understanding of its role in the etiology of multiple diseases. However, the ability to use these recent molecular discoveries to better understand the physiology and pathophysiology of the mitochondria is limited. This is largely due to the lack of research tools and technologies to report on critical mitochondrial signals and processes under physiologically relevant conditions. This particular challenge is at the core of my work.
In my lab, we develop and deploy cutting-edge biophysical and high-resolution imaging techniques that allow us to study mitochondrial ion channels, transporters, and signaling pathways under conditions that closely mimic the living organism. Our goal is to understand how mitochondrial energy production is tuned across different cell types and how it changes during disease. By revealing these molecular mechanisms, we aim to contribute to the development of new treatment strategies that target mitochondrial systems and processes.
My scientific background is rooted in cardiac cell research, where mitochondria are the predominant energy source—occupying more than 30% of the cellular volume, the highest among all mammalian cells. This makes cardiomyocytes an ideal environment to study mitochondrial physiology and pathophysiology.
In 2024, I was awarded a British Heart Foundation Intermediate Fellowship. Shortly thereafter, I relocated my research program from the University of Maryland and joined the Department of Physiology, Anatomy and Genetics, University of Oxford. As a group leader, my team investigates localized sub-cellular signaling systems that regulate mitochondrial ATP production in the heart, and how their pathological changes can lead to energetic deficits in the failing heart.
Key publications
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Voltage-energized calcium-sensitive ATP production by mitochondria
Journal article
Wescott AP. et al, (2019), Nature Metabolism, 1, 975 - 984
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Calcium and bicarbonate signaling pathways have pivotal, resonating roles in matching ATP production to demand
Journal article
Greiser M. et al, (2023), eLife, 12
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Regulation of Mitochondrial ATP Production: Ca2+ Signaling and Quality Control
Journal article
Boyman L. et al, (2020), Trends in Molecular Medicine, 26, 21 - 39
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How the mitochondrial calcium uniporter complex (MCU cx ) works
Journal article
Boyman L. and Lederer WJ., (2020), Proceedings of the National Academy of Sciences, 117, 22634 - 22636
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Ryanodine receptor stabilization therapy suppresses Ca2+- based arrhythmias in a novel model of metabolic HFpEF
Journal article
Kaplan AD. et al, (2024), Journal of Molecular and Cellular Cardiology, 195, 68 - 72
Recent publications
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Constitutive deletion of the obscurin-Ig58/59 domains induces atrial remodeling and Ca2+-based arrhythmogenesis.
Journal article
Grogan A. et al, (2025), JCI Insight, 10
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Outer mitochondrial membrane E3 Ub ligase MARCH5 controls de novo peroxisome biogenesis
Journal article
Verhoeven N. et al, (2025), Developmental Cell, 60, 40 - 50.e5
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Ryanodine receptor stabilization therapy suppresses Ca2+- based arrhythmias in a novel model of metabolic HFpEF
Journal article
Kaplan AD. et al, (2024), Journal of Molecular and Cellular Cardiology, 195, 68 - 72
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Na+/K+ATPase-Cav1.2 nanodomain differentially regulates intracellular [Na+], [Ca2+] and local adrenergic signaling in cardiac myocytes
Preprint
Karbowski M. et al, (2023)
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Outer mitochondrial membrane E3 Ub ligase MARCH5 controls mitochondrial steps in peroxisome biogenesis
Preprint
Verhoeven N. et al, (2023)

