Regulation and role of calcium in cellular senescence

Abstract

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.

Keywords: Aging; Calcium; Cancer; Mitochondria-ER contacts; Senescence; Signaling.