Regulation and role of calcium in cellular senescence

Cellular senescence is a state of stable cell proliferation arrest accompanied by a distinct secretory program impacting the senescent cell microenvironment. This phenotype can be induced by many stresses, including telomere shortening, oncogene activation, oxidative or genotoxic stress. Cellular senescence plays a key role in the organism throughout life, with beneficial effects at a young age for instance in embryonic development and wound healing, and deleterious effects during aging and in aging-related diseases. In the last decade calcium and calcium signaling have been established as critical factors in the implementation and regulation of cellular senescence. In this review we will present and discuss the main discoveries in this field, from the observation of an increased intracellular calcium concentration in senescent cells to the identification of calcium-binding proteins, calcium channels (TRP, ITPR, ...) and MERCs (mitochondria-endoplasmic reticulum contact sites) as key players in this context.

Automated summary

Cellular senescence is a state of cell proliferation arrest accompanied by a specific secretory program, which affects the microenvironment of senescent cells. Various stresses can induce cellular senescence, such as telomere shortening, oncogene activation, oxidative or genotoxic stress. Cellular senescence plays a crucial role throughout life, showing beneficial effects in embryonic development and wound healing, but also detrimental effects in aging and aging-related diseases. In recent years, calcium and calcium signaling have been identified as critical factors in the implementation and regulation of cellular senescence. This review highlights the main discoveries in this field, including the increased intracellular calcium concentration in senescent cells, the identification of calcium-binding proteins, calcium channels (TRP, ITPR, ...), and MERCs (mitochondria-endoplasmic reticulum contact sites) as key players in this context.