Our Mission
We aim to understand the mechanisms controling myofibroblast function and how they influence the development of fibrosis. We carry out functional analysis of the cell's contractile apparatus (actin stress fibers), of force transmission at sites of cell-extracellular matrix contacts (focal adhesions) and of the mechanical cross-talk between contractile stress fibers of contacting fibroblasts at sites of cell-cell adherens junctions. We develop novel strategies to counteract myofibroblast malfunction by targeting these instrumental structures of the contractile phenotype.
Our Research
Myofibroblasts restore connective tissue integrity and contract the wound during tissue repair. Excessive myofibroblast activity is characteristic of the majority of fibrocontractive diseases. Following tissue injury, local fibroblasts and other mesenchymal cells, blood-circulating cells, epithelial and endothelial cells acquire smooth muscle features. Hallmark of this transition is the neo-expression of α-smooth muscle actin, generating high contractile activity in stress fibres. Of clinical relevance are the retractile phenomena caused by excessive myofibroblast activity characterizing the vast majority of fibrocontractive diseases. This includes fibrosis affecting vital organs, such as heart, liver, kidney and lung.
Our Tools
At LTRR, we develop and use state of the art equipment for analyzing mechanical forces in vivo and in vitro and performing high sensitivity fluorescence microscopy. We specialize in analyzing and measuring forces on the level of subcellular structures (contact sites), of individual cells, of cell populations and ex vivo tissue samples.