Calcium signaling and cellular senescence
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Nadine Martin1, David Bernard1
1Inserm U1052, Centre de Recherche en Cancérologie de Lyon, F-69373 Lyon, France; CNRS UMR 5286, F-69373 Lyon, France; Centre Léon Bérard, F-69373 Lyon, France; Université de Lyon, F-69373 Lyon, France.
Abstract:
Cellular senescence is a stable cell proliferation arrest induced by a variety of stresses including telomere shortening, oncogene activation and oxidative stress. This process plays a crucial role in many physiopathological contexts, especially during aging when cellular senescence favors development of age-related diseases, shortening lifespan. However, the molecular and cellular mechanisms controlling senescence are still a matter of active research. In the last decade, there has been emerging literature indicating a key involvement of calcium signaling in cellular senescence. In this review we will initially give an account of the direct evidence linking calcium and the regulation of senescence. We will then review our current knowledge on the role of calcium in some senescence-associated features and physiopathological conditions, which will shed light on additional ways in which calcium signaling is implicated in cellular senescence.