Andia Redpath

Project: Targeting cardiac mesothelium to dampen inflammation in non-infectious carditis

Research summary

Inflammatory cardiac disorders – myocarditis and pericarditis – often develop due to viral or bacterial infections, and these infectious causes take centre stage in research. The clinical incidence of infection-driven carditis may significantly outweigh non-infectious aetiologies, however this should not reduce the need to understand pathogenesis due to less common causes. Immunological disorders, such as systemic lupus erythematosus (SLE), and cardiovascular disease, such as acute myocardial infarction with reduced ejection fraction (HFrEF) may demonstrate sustained cardiac autoimmunity. Research studies into the pathogenesis of autoimmune myocarditis focus on the immune system and consequent tissue damage, however, have not investigated the participation of the cardiac mesothelium (epicardium). My research will focus on the epicardium and its participation in the immune response and disease pathogenesis.  

Background

During my graduate studies at Imperial College London, I engaged in a variety of research from vascular to bone replacement therapeutics, before committing to a PhD project targeting endogenous somatic progenitor cells (haematopoietic and mesenchymal) to employ their regenerative properties. My passion for improving therapeutic targets using discoveries from basic research led me to my postdoctoral work with Prof. Nicola Smart at the University of Oxford. Our research centred around re-activation of developmental programmes to achieve regeneration of the infarcted heart. I gained extensive expertise on the cardiac mesothelium and cell signalling in development, health and disease. To attain my research independence and further my interests in the cardiac mesothelium in disease, I have developed an independent research topic to investigate its roles in non-infectious carditis pathogenesis. Only a handful of studies have investigated the role of pericardial compartments in disease models, predominantly in ischaemic injury (myocardial infarction), and found that the mesothelium potentially has both pro-inflammatory and immunomodulatory characteristics. The research supported by the BHF CRE Fellowship will interrogate mesothelial-immune cell interactions to yield ways of targeting and reprogramming the inflammatory microenvironment. My interests in targeting the mesothelium for cardioprotection and repair is supported by experts in the field, Prof. Paul Riley (sponsor, mentor) and Prof. Nicola Smart (collaborator, mentor), and our collaboration will enable me to uncover its role in cardiac autoimmunity and chronic inflammation.