Abstract
Cells sense and transmit mechanical forces exerted by their environment to the nucleus via adhesion sites and the cytoskeleton. The nucleus interprets these mechanical inputs and determines cell fate and behavior by regulating gene expression. This review addresses how force-generated signals at the cell-extracellular matrix (ECM) interface influence adhesion, signaling, nuclear function, and tissue remodeling. Disruption of these mechanotransduction pathways contributes to the development of diseases such as cancer, fibrosis, and cardiovascular disorders. Advances in technologies that enable the investigation of the underlying mechanisms will support the development of novel treatment strategies for such diseases.