Contact information
Websites
Christopher Toepfer
PhD
Associate Professor of Cardiovascular Science
- Sir Henry Dale Fellow
- BHF CRE Intermediate Transition Fellow
- Eugene Braunwald Fellowship in Cardiovascular Medicine 2018-2019 BWH
Background
Chris completed his PhD at Imperial College London under the supervision of Professor Michael Ferenczi and Dr. James Sellers (NHLBI, NIH). Studying cardiac muscle regulation in health and disease. He subsequently began a Post-doc with the support of a Sir Henry Wellcome Post-Doctoral Fellowship with Professors Christine and Jonathan Seidman at Harvard Medical School and Professor Hugh Watkins at the RDM Oxford.
Chris is currently supported by a BHF CRE Intermediate Transition Fellowship In Oxford to investigate the role of thick filament variants in hypertrophic cardiomyopathy (HCM). The laboratory focuses on CRISPR/Cas-9 engineering of human induced pluripotent stem cells. These cells can be differentiated into cardiomyocytes, which are used to model human heart disease in a dish.
In the Press and Editorials
- BBC website 'Cancer treatment broke my heart, but I've survived'
- Nature Reviews Cardiology Editorial ‘Modulating myosin function to treat hypertrophic cardiomyopathy’
- Circulation Editorial ‘Manipulating Myosin May Help Treat Hypertrophic Cardiomyopathy’
- Circulation Research Editorial ‘High-Throughput Contractility Assay for Human Stem Cell-Derived Cardiomyocytes: One Beat Closer to Tracking Heart Muscle Dynamics’
- HMS press release and interview ‘On the Beat’
- HMS press release and interview ‘Bad Brakes’
- HMS press release and interview 'Revving the engine'
Recent publications
ssaying the myosin super-relaxed state across muscle types, cells and proteins for understanding muscle biology and use in drug discovery.
Journal article
Jones STM. et al, (2025), Nat Protoc
Microscale droplet assembly enables biocompatible multifunctional modular iontronics.
Journal article
Zhang Y. et al, (2024), Science, 386, 1024 - 1030
Hypertrophic cardiomyopathy-associated mutations drive stromal activation via EGFR-mediated paracrine signaling.
Journal article
Ewoldt JK. et al, (2024), Sci Adv, 10
n ALPK3 truncation variant causing autosomal dominant hypertrophic cardiomyopathy is partially rescued by mavacamten
Preprint
Leinhos L. et al, (2024)
Targeted genetic therapies for inherited disorders that affect both cardiac and skeletal muscle.
Journal article
Psaras Y. and Toepfer CN., (2024), Exp Physiol, 109, 175 - 189
Comparing the effects of chemical Ca2+ dyes and R-GECO on contractility and Ca2+ transients in adult and human iPSC cardiomyocytes.
Journal article
Robinson P. et al, (2023), J Mol Cell Cardiol, 180, 44 - 57
Mechanism based therapies enable personalised treatment of hypertrophic cardiomyopathy.
Journal article
Margara F. et al, (2022), Sci Rep, 12
