Integrin-linked kinase (ILK) is a protein located in focal adhesion complexes that is linked to the cytoplasmic domain of integrin receptors. Together with PINCH and parvin, ILK forms the IPP complex, which is associated with conserved intracellular signalling pathways and integrin regulation of the actin cytoskeleton. ILK plays an essential role in a wide variety of cellular functions, including cell migration, differentiation, survival, and division. The present review summarizes recent evidence, suggesting a new role for ILK in organismal ageing and cellular senescence, indicating that ILK is a key regulator of longevity and premature cellular senescence induced by extracellular stressors.Graphical abstract
Schematic representation of ILK implication in ageing. (Upper panel) Cellular senescence. Physiological context: ILK is overexpressed in cells from old mice, inducing senescent genes (Chen et al., 2006). Pathological context: ILK is overexpressed in cancer cells, and its repression induces senescence (Zhu et al., 2014 and Duminuco et al., 2015). Some extracellular stressors such as ROS and hyperphosphatemia induce senescence through ILK activation (Troyano et al., 2015; Troyano-Suárez et al., 2015). (Lower panel) Organismal Ageing. Old or hyperphosphatemic animals show increased ILK (Troyano et al., 2015; Troyano-Suárez et al., 2015). Moderate repression (├) or strong repression (╟) of ILK induce different consequences in organisms (Kumsta et al., 2014; Nishimura et al., 2014).