Can mechanical forces attune heterotypic cell-cell communications?
Heterotypic cell lineages relentlessly exchange biomechanical signals among themselves in metazoan organs. Hence, cell-cell communications are pivotal for organ physiology and pathogenesis. Every cell lineage of an organ responds differently to a specific signal due to its unique receptibility and signal interpretation capacity. These distinct cellular responses generate a system-scale signaling network that helps in generating a specific organ phenotype. Although the reciprocal biochemical signal exchange between non-identical neighboring cells is known to be an essential factor for organ functioning, if, then how, mechanical cues incite these signals is not yet quite explored. Cells within organ tissues experience multiple mechanical forces, such as stretching, bending, compression, and shear stress. Forms and magnitudes of mechanical forces influence biochemical signaling in a cell-specific manner. Additionally, the biophysical state of acellular extracellular matrix (ECM) can transmit exclusive mechanical cues to specific cells of an organ. As it scaffolds heterotypic cells and tissues in close proximities, therefore, ECM can easily be contemplated as a mechanical conduit for signal exchange among them. However, force-stimulated signal transduction is not always physiological, aberrant force sensing by tissue-resident cells can transduce anomalous signals to each other, and potentially can promote pathological phenotypes. Herein, I attempt to put forward a perspective on how mechanical forces may influence signal transductions among heterotypic cell populations and how they feedback each other to achieve a transient or perpetual alteration in metazoan organs. A mechanistic insight of organ scale mechanotransduction can emanate the possibility of finding potential biomarkers and novel therapeutic strategies to deal with pathogenesis and organ regeneration.