Cardiometabolic Disease

Current research projects

• Human cardiorenal co-culture model of diabetic cardiorenal syndrome

  Cardiorenal syndrome, or cardiovascular–kidney–metabolic (CKM) syndrome, describes the bidirectional relationship between heart and kidney dysfunction, yet no human experimental model currently exists to study this interaction under disease conditions. We are developing a stem cell-derived cardiorenal co-culture system that brings together cardiac and kidney organoids to model how metabolic stress, particularly in the context of diabetes, drives simultaneous organ dysfunction. This platform enables real-time functional assessment of both tissues, with the capacity to extend to other cardiorenal disease contexts including hypertension and drug-induced cardio- and nephrotoxicity.

  Diabetic cardiomyopathy: mechanisms and therapeutic targets

  Diabetes is a leading cause of heart failure, yet the mechanisms by which chronic metabolic stress drives cardiac dysfunction remain incompletely understood. Using human iPSC-derived cardiac microtissues exposed to diabetic conditions, we are investigating the cellular and molecular pathways underlying diabetic cardiomyopathy. This program aims to identify mechanisms for intervention and to test candidate therapies in a human experimental system that reflects the complexity of the diabetic heart.

  Friedreich ataxia cardiomyopathy: mRNA therapies

  Friedreich ataxia is a rare multisystem disease, caused by reduced expression of frataxin, a mitochondrial protein essential for iron-sulphur cluster assembly and respiratory chain function. Cardiac disease is the leading cause of death in affected individuals, yet no cardiac therapy currently exists. We are developing and testing mRNA-based strategies to restore cardiac function in patient-derived iPSC cardiac models, assessing functional rescue across contractility, electrophysiology, and mitochondrial endpoints.

  Untangling the cardiac lipidome in Friedreich ataxia

  Friedreich ataxia is associated with significant dysregulation of the cardiac lipidome, yet the functional consequences of these changes and their therapeutic potential remain poorly characterised. In collaboration with the Baker Heart and Diabetes Institute, we apply lipidomic profiling to patient-derived cardiac microtissue models to identify disease-associated lipid signatures and candidate therapeutic targets. Novel lipid-based agents are then tested in our stem cell-derived cardiac models, providing a human experimental platform to evaluate their capacity to restore lipid homeostasis and improve cardiac function in Friedreich ataxia.