Eva Faurobert

This study investigates how loss of CCM2 disrupts endothelial force balance in cerebral cavernous malformations by analyzing molecular forces and adhesion organization.

This study identifies PIEZO1, TRPV2, and TRPV4 as mechanosensors overexpressed in CCM lesions, showing their role in driving disease through altered adhesion and matrix degradation.

This study uses optogenetic tools to reveal distinct functional roles of SRC and HCK kinases in macrophages, despite their redundancy.

This study reveals how CCM2-silenced endothelial cells use mechanical forces to recruit and reprogram wild-type cells, driving vascular lesion growth through force-guided invasion and cellular reprogramming.