The regulation of mechanosensing in healthy and atherosclerotic VSMC

Vascular smooth muscle cellsplay a central role in the onset and progression of many cardiovascular diseases, from atherosclerosis to vascular injury, where their migration, matrix secretion, or degradation functions are deregulated. Here we are investigating how the phenotypic switch is regulated through physical/mechanical stimuli.

3D Photoelectrochemical Imaging in Porous Light-Addressable Structures

Investigating the cardiomyocyte rigidity sensing mechanism with micro patterned surfaces and nanopil

The composition and the stiffness of the cardiac extracellular matrix change during development or in heart disease. Cardiomyocytes and their progenitors sense these changes, which decides over Cardiomyocyte fate. Our preliminary data suggested a cardiomyocyte specific rigidity sensing mechanism which we will investigate here in detail.

Mechano-regulation of myofibril formation and cardiac remodelling

While chemical cues have well-established roles in guiding cell differentiation, there is growing evidence of a role for mechanical stimuli, such as matrix rigidity during heart development and disease. However, the mechanisms that underlie this mechanical signalling remain elusive. Here we will study this by combining cell biology, biophysics and nanotechnology in a three-tiered approach in which we examine the cardiomyocyte response to A) passive resistance and varying rigidity; B) active force; C) no force. Detailed understanding will lead to novel and valuable insights into mechanisms of cardiac mechanosensing and could result in novel or improved therapeutic strategies for cardiac diseases.