Hans Van Oosterwyck

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 paper investigates how matrix stiffness and shear stress jointly influence endothelial gene expression and angiogenic activation thresholds using transcriptomics.

This study combines Traction Force Microscopy and Vinculin Tension Sensors to analyze how molecular tension and cellular tractions interact across different scales in focal adhesions.

This study shows that microtubule detyrosination promotes directional migration and matrix remodeling during endothelial sprouting by enhancing ECM degradation and force transmission.

This study shows OA chondrocytes generate higher contractile forces in 3D degradable hydrogels compared to 2D, linked to increased protrusive activity and actomyosin engagement.

This paper introduces DD-TFM, a data-driven 3D traction force microscopy method that models collagen hydrogels as discrete fiber networks, revealing fiber-level matrix deformations caused by endothelial cells.

This study shows LOXL2 mediates BM assembly in response to microenvironment topography, affecting endothelial cell behavior and barrier properties.

This paper introduces an inverse methodology for 3DTFM to reconstruct spatially heterogeneous ECM stiffness distributions, validated using in silico cases and compared to L-BFGS.

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.

The paper develops a computational model of endothelial cell migration during vascular remodelling, showing shear stress and cell elongation are key factors.