Marta Moya Jódar

Dr. Moya-Jódar’s research focuses on understanding how cardiac disease emerges from disrupted cellular and multicellular processes, and how this knowledge can be translated into effective therapeutic strategies. Her work focuses on Friedreich’s ataxia (FRDA), a rare genetic disorder in which cardiomyopathy is the leading cause of mortality, yet remains poorly understood at the tissue and systems levels.

By combining human-relevant cardiac models with functional and molecular analyses, she seeks to define disease-driving mechanisms underlying FRDA-associated cardiomyopathy and to identify opportunities to preserve cardiac function.

Dr. Moya-Jódar is a postdoctoral researcher in the Toepfer Group within the Division of Cardiovascular Medicine (CVM) at the University of Oxford. Her research focuses on modelling Friedreich’s ataxia–associated cardiomyopathy using human induced pluripotent stem cell (iPSC)–derived cardiac systems.

Her work integrates patient-derived cardiomyocytes with multicellular cardiac models to investigate how disrupted intercellular communication and tissue organisation contribute to disease progression. Through this approach, she aims to bridge mechanistic insight with translational relevance, informing the development of future therapeutic strategies for FRDA-associated cardiomyopathy.

Prior to joining the University of Oxford, Dr. Moya-Jódar completed her doctoral and postdoctoral training in the Department of Regenerative Medicine at CIMA–Universidad de Navarra (Spain). There, she specialised in the naïve conversion of human induced pluripotent stem cells (hiPSCs) and their application in developmental biology, including human-animal chimera models.

This work focused on understanding early developmental potential and cell fate decisions, providing a strong foundation for her current research interest in how developmental processes and cell-cell interactions shape cardiac disease. She now applies this developmental perspective to human cardiac disease modelling, with a focus on FRDA-associated cardiomyopathy.