DBC Symposium with Otto Wolff Lecture
Join us for a one-day in-person symposium filled with engaging presentations and discussion from the department's early career researchers, before concluding with the Otto Wolff Lecture.
Join us for a one-day in-person symposium filled with engaging presentations and discussion from the department’s early career researchers, celebrating UCL’s bicentenary, before concluding with the Otto Wolff Lecture. The symposium is open to all members from the Department of Developmental Biology and Cancer, while the Otto Wolff Lecture is open to all staff and students based at the UCL GOS ICH. The programme will be announced closer to the event date. The event is fully catered and will conclude with a drink social from 17:00-19:00 (location TBC).
Registration is Open
Registration for this year’s symposium is now open. To register, please follow this link. Please state any dietary and accessibility requirements in the pop-up box following registration.
Registration deadline is Friday 10th April 2026.
Otto Wolff Lecture
Cardiac Lymphatics in Heart Repair and Regeneration
Heart attack or myocardial infarction (MI) triggers an immune response; whereby phagocytic cells (such as macrophages) remove dead tissue and assist with subsequent repair. High load and persistence of immune cells, however, contributes to further fibrosis, pathological remodelling and ultimately progression to heart failure. We have shown that the adult cardiac lymphatics traffic macrophages to draining mediastinal lymph nodes post-MI, and this can be augmented by invoking lymphangiogenesis through VEGFC-treatment to effect optimal repair and improve function. We have further identified which subsets of VEGFC-cleared macrophages correlate with improved outcome, alongside molecular changes in the lymphatic endothelium that evoke specific immune cell clearance. In parallel, we have investigated the role of the cardiac lymphatics across the regenerative window in neonatal mice (post-natal days 1-7; P1-P7). The response to injury differs significantly in P1 versus P7 hearts, with decreased lymphangiogenesis and minimal clearance of macrophages at P1, consistent with the need to maintain a pro-regenerative population. scRNA-Seq reveals differences in cellular crosstalk across the regenerative window and in mice lacking lymphatic endothelial receptor-1 (Lyve1) we surprisingly observed impaired functional outcome in P1 infarcted hearts. This is underpinned by a shift in the balance of pro-regenerative tissue resident macrophages to pro-inflammatory monocytes. Pilot data suggests Lyve-1 maintains the glycocalyx (“pericellular matrix”) of tissue resident macrophages shielding them from apoptotic “eat-me” signals to facilitate neonatal heart regeneration.
Biography
Paul Riley is the British Heart Foundation Professor of Regenerative Medicine based at the University of Oxford where he is also the Chair of Development & Cell Biology within the Department of Physiology, Anatomy & Genetics. He is the inaugural Director of the Institute of Developmental and Regenerative Medicine (IDRM) which came online in May 2022 and Co-Director of the MRC/BHF Centre of Research Excellence in Advanced Cardiac Therapies (REACT) which started in January 2025. He was formerly Professor of Molecular Cardiology at the UCL-Institute of Child Health, London, where he was a principal investigator within the Molecular Medicine Unit for 12 years. Prior to this, he obtained his PhD at UCL and completed post-doctoral fellowships in Toronto and Oxford.
In 2008, Professor Riley was awarded an Outstanding Achievement Award by the European Society of Cardiology, in recognition of his team’s discovery that activated epicardial cells can regenerate the adult mammalian heart, and in 2014 he was elected a fellow of the Academy of Medical Sciences.
His research interests span across multiple aspects of cardiovascular development and modelling congenital heart disease, alongside how to restore embryonic potential and condition the local environment in the injured/diseased adult heart to facilitate optimal repair and regeneration.