After the onset of ischaemia, hypoxia-related pathways, immunoinflammatory balance, as well as changes in hemodynamical forces within vascular wall trigger all the processes regulating vascular homeostasis, including vasculogenesis, angiogenesis, arteriogenesis which act in concert to establish a functional vascular network in ischaemic zones. In patients with ischemic diseases, most of the cellular and molecular mechanisms involved in the activation of vessel growth and vascular remodelling are markedly compromised. Moreover, impaired endothelial function due to cardiovascular risk factors such as obesity and diabetes leads to development and rapid progression of severe vascular diseases. Thus, the identification and characterization of novel genes/regulatory pathways to better understand the process behind vascular repair is therefore crucial.

My lab aims to unravel the complexity behind vascular signalling during post-ischaemic angiogenesis and vascular repair.  As a lab, we favour a general view that dysregulation of basal ECs function, including that during hypoxia/ischaemia, arises from dysregulation of intra-cellular and inter-cellular communication. These processes could significantly influence the mechanisms of vascular signalling. We use a combination of the cutting-edge techniques and approaches, including high-content screen and RNA sequencing whereby we identified new vascular targets and defined their role of during angiogenesis process and vascular regeneration. Moreover, by performing loss-of-function studies and pre-clinical imaging we are able to characterize the impact of selected pathways on capillary growth or collateralization in vivo.