Damage accumulation in long-living macromolecules, especially extracellular matrix proteins, is highly connected to aging and mortality. Mechano-sensitive integrins that interact with the matrix are involved in intercellular contacts, wound healing, degenerative diseases of cartilage, fibrosis and cancer. Cross-linking and stiffening of ECM aging leads to immunodeficiency and cardiac dysfunction, also being a characteristic sign of lung fibrosis during aging.
We aim to create a platform for potential treatment development to decrease and reverse ECM stiffening or its pathological signalling into the cell.