Dr Rebecca Gilchrist

  • Research Associate (School of Cardiovascular & Metabolic Health)

email: Rebecca.Gilchrist@glasgow.ac.uk
pronouns: She/her/hers

Sir James Black building, room 419, School of Cardiovascular & Metabolic Health, University of Glasgow, Glasgow, UK, G12 8QQ

Import to contacts

ORCID iDhttps://orcid.org/0000-0001-5003-4362

Biography

Rebecca studied Natural Sciences at the University of Cambridge, specialising in Pharmacology, before moving back to Glasgow to complete a Master of Research in Translational Medicine as part of the BHF 4-year PhD programme. During her PhD, she researched mechanisms of ventricular arrhythmia in long QT syndrome, working under the supervision of Professor Rachel Myles, Professor Godfrey Smith and Dr Francis Burton. She now works as a Research Associate in Professor Will Fuller’s lab, and her current research aims to determine whether strategic post-translational modulation of cardiac ion channels could provide inotropic and anti-arrhythmic effects in the setting of heart failure. Rebecca is a member of the Heart Rhythm Society, British Heart Rhythm Society and the Physiological Society, and was recently awarded the British Heart Rhythm Society Young Investigator Award.

Research interests

Reasearch Theme: Cardiac

Rebecca’s interests include understanding how normal cardiac physiology becomes altered in disease and, more specifically, how this knowledge can be leveraged to develop novel risk stratification and treatment approaches. During her PhD, she became particularly interested in ventricular arrhythmia mechanisms and in the physiological and potential pathological implications of cardiac memory. She has extensive experience using optical recordings of transmembrane voltage in Langendorff-perfused hearts and large populations of isolated cardiomyocytes to examine ventricular arrhythmia mechanisms under long QT conditions. In her current role, Rebecca uses various biochemical techniques, cell lines and human induced pluripotent stem cell-derived cardiomyocytes to examine whether targeting post-translational regulation of cardiac ion channels could provide beneficial inotropic and anti-arrhythmic effects in heart failure.

Publications

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