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.
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
The curious case of dermal fibroblasts: cell identity loss may be a mechanism underlying cardiovascular aging.
Badi I., (2019), Cardiovasc Res, 115, e24 - e25
miR-34a Promotes Vascular Smooth Muscle Cell Calcification by Downregulating SIRT1 (Sirtuin 1) and Axl (AXL Receptor Tyrosine Kinase).
Badi I. et al, (2018), Arterioscler Thromb Vasc Biol, 38, 2079 - 2090
MicroRNA-34a modulates vascular calcification
Badi I. et al, (2018), VASCULAR PHARMACOLOGY, 103, 62 - 62
Non-oxidizable HMGB1 induces cardiac fibroblasts migration via CXCR4 in a CXCL12-independent manner and worsens tissue remodeling after myocardial infarction.
Di Maggio S. et al, (2017), Biochim Biophys Acta Mol Basis Dis, 1863, 2693 - 2704