- Riley Group Research Group
Postdoctoral Research Scientist
Joaquim Vieira studied biochemistry at the University of Lisbon, Portugal. He then moved to London for his PhD studies on the role of neuropilin 1 (NRP1) and its ligands during blood vessel growth and patterning in Professor Christiana Ruhrberg's laboratory at the University College London (UCL)-Institute of Ophthalmology. In 2008, Joaquim started as a postdoctoral researcher at the UCL-Institute of Child Health in Professor Paul Riley's laboratory to work on the charaterisation of adult epicardium-derived cells (EPDCs) and their contribution to cardiovascular homeostasis and endogenous repair. Joaquim joined the Department in June 2012 as part of the move of the "Riley lab" to Oxford. Joaquim is also a Fulford Junior Research Fellow (JRF) at Somerville College since October 2013.
Joaquim's current research interests include investigating the epigenetic mechanism(s) controlling epicardial activity during heart development and disease; and characterisation of small molecules with cardiogenic potential.
De novo cardiomyocytes from within the activated adult heart after injury.
Smart N. et al, (2011), Nature, 474, 640 - 644
Tissue macrophages act as cellular chaperones for vascular anastomosis downstream of VEGF-mediated endothelial tip cell induction.
Fantin A. et al, (2010), Blood, 116, 829 - 840
Selective requirements for NRP1 ligands during neurovascular patterning.
Vieira JM. et al, (2007), Development, 134, 1833 - 1843
Regulation of embryonic neurogenesis by germinal zone vasculature
Tata M. et al, (2016), Proceedings of the National Academy of Sciences, 113, 13414 - 13419
Characterisation of the human embryonic and foetal epicardium during heart development.
Risebro CA. et al, (2015), Development, 142, 3630 - 3636
Cardiac lymphatics are heterogeneous in origin and respond to injury.
Klotz L. et al, (2015), Nature, 522, 62 - 67
Re-activated adult epicardial progenitor cells are a heterogeneous population molecularly distinct from their embryonic counterparts.
Bollini S. et al, (2014), Stem Cells Dev, 23, 1719 - 1730
Loss of Prox1 in striated muscle causes slow to fast skeletal muscle fiber conversion and dilated cardiomyopathy.
Petchey LK. et al, (2014), Proc Natl Acad Sci U S A, 111, 9515 - 9520