I have been involved in the research for Hereditary Hemorrhagic Telangiectasia since 2005. HHT is a vascular disorder caused by mutations in Alk1 and Endoglin, both endothelial receptors of TGFbeta. The pathology is characterized by aberrant direct connections in between arteries and veins called arteriovenous malformations. These AVMs appear in the skin and internal organs of the patients, leading to nose and GI tract bleedings, and they could be lethal if occur in the brain. During my PhD, I studied the molecular pathways affected in the disease, working with cell cultures of primary endothelial cells obtained from the patients, and performing multiple in vitro experiments.I studied the transcriptional regulation of the promoters of these proteins, as well as protein interactions and phosphorylation state of the TGFbeta - Alk1/Eng - Smads cascade. For my postdoctoral training I moved to one of the top laboratories in HHT field, to get even more specialized on the disease. Here I am studying the molecular mechanisms that lead to the developing of arteriovenous malformations working in vivo with the mouse model of the disease. I have generated induced pluripotent stem cells, and differentiated them to endothelial and smooth muscle cells to study the properties of these cells in terms of tube formation and vascular differentiation between mutant and control cells in vitro. I am also applying hyper spectral imaging techniques to track the formation of the AMVs in a window chamber installed in the skin of the mouse, and trying several drugs to try to prevent and reverse the formation of the AVMs in vivo.