Defining the role mechanical forces play in determining cell identity and function is imperative to interpreting cellular and physiological phenomena, as well as inspiring the development of novel therapeutics. As the field of mechanotransduction has grown in size and appreciation, there have been great strides in defining the molecular mechanisms by which cells respond to their mechanical environment. This includes characterization of the interface between the cell's surface and the extracellular matrix (ECM) via integrin-based adhesions, as well as a deeper understanding of the nucleus as a force sensor capable of driving changes to gene expression. However, disentangling mechanosensitive cellular pathways has proven challenging, particularly defining if and how characterized cellular mechanosensors work in parallel or in unison. In this review, we will highlight the interplay between integrin-ECM adhesions and the nucleus, summarizing what is currently understood about how mechanical information is relayed and integrated across these two mechanoresponsive entities.
Sandria et al. (Thu,) studied this question.