Senior Postdoctoral Researcher
My principal research interests lie in understanding the cellular and molecular mechanisms leading to cardiovascular disease. I obtained my Ph.D. in 2008 at the University of Insubria (Italy), where I studied the role of the transcription factor Ankrd1 in the pathogenesis of the rare congenital heart disease Total Anomalous Pulmonary Venous Return (TAPVR). Hence, I decided to deepen my knowledge on the transcriptional control of cardiac development in Professor Vincent M. Christoffels’s lab at the University of Amsterdam. There, I studied the transcriptional regulation of Tbx3 gene that encodes a transcription factor important for the conduction system and arterial pole morphogenesis. At this point I felt the need to move towards more translational studies; thus, I spent six years at the Centro Cardiologico Monzino, in Milan, where I focused my attention on the role of miR-34a in vascular “inflammaging” and vascular calcification, as this microRNA could be a promising therapeutic target for cardiovascular disease. In June 2018 I joined The Oxford Translational Cardiovascular Research Group, that superbly combines basic science and clinical research. Here, I am keen on studying how the cross-talk between adipose tissue and the cardiovascular system can affect cardiovascular disease.
Myocardial overexpression of ANKRD1 causes sinus venosus defects and progressive diastolic dysfunction.
Piroddi N. et al, (2019), Cardiovasc Res
Myocardial redox state predicts 3-year mortality in patients undergoing cardiac surgery: the ox-HVF study
Kotanidis C. et al, (2019), EUROPEAN HEART JOURNAL, 40, 3886 - 3886
Novel direct effects of SGLT2 inhibitor, Canagliflozin, on myocardial redox state in humans
Kondo H. et al, (2019), EUROPEAN HEART JOURNAL, 40, 3872 - 3872
Wnt5a contributes to human atherosclerosis via novel USP17 redox signalling
Akoumianakis I. et al, (2019), EUROPEAN HEART JOURNAL, 40, 1660 - 1660
Adipose tissue-derived WNT5A regulates vascular redox signaling in obesity via USP17/RAC1-mediated activation of NADPH oxidases.
Akoumianakis I. et al, (2019), Sci Transl Med, 11