BHF Intermediate Fellow and Associate Professor
My research revolves around metabolism and the heart – understanding why metabolism is important and what the consequences are when it goes wrong.
My passion for metabolism began during my undergraduate degree in Medical Biochemistry at the University of Surrey. I loved the way everything fitted together into this complex jigsaw, which in many ways resembled the London Underground map. And just like a public transport network, if something goes wrong with one enzyme or pathway, the whole system can either adapt or grind to a halt.
My doctoral research investigated the role of abnormal substrate metabolism in the development of cardiac hypertrophy. My subsequent post-doctoral research focused on the role of mitochondrial metabolism in cardiac disease progression.
In 2011 I was awarded a Diabetes UK RD Lawrence Fellowship, to study the role of hypoxia and metabolism in the type 2 diabetic heart. Heart disease is the leading cause of mortality in patients with type 2 diabetes, and patients have increased incidence of, and decreased recovery following myocardial infarction.
In 2018 I was awarded a British Heart Foundation Intermediate Fellowship, to study why fat accumulation in the type 2 diabetic heart is such a bad thing. We are studying what fats can do to the function of the cardiomyocyte, and how they might be signalling to activate deleterious processes. We have identified a number of novel signalling roles for fatty acids within the diabetic myocardium - regulating transcription factors, post-translational modifications and competitively inhibiting enzymes - that contribute to cardiomyocyte dysfunction at rest and in response to stress in type 2 diabetes.
Activation of HIF1α Rescues the Hypoxic Response and Reverses Metabolic Dysfunction in the Diabetic Heart.
da Luz Sousa Fialho M. et al, (2021), Diabetes
Rescue of myocardial energetic dysfunction in diabetes through the correction of mitochondrial hyperacetylation by honokiol.
Kerr M. et al, (2020), JCI Insight, 5
Fatty acids prevent Hypoxia-Inducible Factor 1α signalling through decreased succinate in diabetes
Heather L. et al, (2018), JACC: Basic to Translational Science
Inhibition of sarcolemmal FAT/CD36 by sulfo-N-succinimidyl oleate rapidly corrects metabolism and restores function in the diabetic heart following hypoxia/reoxygenation.
Mansor LS. et al, (2017), Cardiovascular Research
Increased oxidative metabolism following hypoxia in the type 2 diabetic heart, despite normal hypoxia signalling and metabolic adaptation.
Heather L. et al, (2015), The Journal of Physiology
Differential translocation of the fatty acid transporter, FAT/CD36, and the glucose transporter, GLUT4, coordinates changes in cardiac substrate metabolism during ischemia and reperfusion.
Heather LC. et al, (2013), Circ Heart Fail, 6, 1058 - 1066