BSc (Hons), MSc, PhD
My research focuses on the changes in calcium handling and contractility that occur in inherited cardiomyopathies. I study mutations in thin filament proteins that cause hypertrophic (HCM) and dilated (DCM) cardiomyopathy. My work has developed myofilament specific genetically encoded calcium sensors for the study of subcellular calcium dynamics in cardiomyocytes expressing HCM and DCM mutations.
My current research is on the development of novel synthesised analogues of epigallocatechin-3-gallate (EGCG), which decrease calcium sensitivity in cardiomyocytes. The aim of which is to provide a safe and effective treatment for patients with HCM.
I completed my PhD at the University of Nottingham in developmental biology where I studied the role of LIM kinase and metanephric mesenchymal cell migration in the developing kidney.
Hypertrophic cardiomyopathy mutations increase myofilament Ca2+ buffering, alter intracellular Ca2+ handling and stimulate Ca2+ dependent signalling.
Robinson P. et al, (2018), J biol chem
LIM kinase function and renal growth: Potential role for LIM kinases in fetal programming of kidney development.
Sparrow AJ. et al, (2017), Life sci, 186, 17 - 24
Acetylsalicylic acid interferes with embryonic kidney growth and development by a prostaglandin-independent mechanism.
Welham SJM. et al, (2017), World j nephrol, 6, 21 - 28
Excess maternal salt intake produces sex-specific hypertension in offspring: putative roles for kidney and gastrointestinal sodium handling.
Gray C. et al, (2013), Plos one, 8