Publications by authors named "Clotilde Raynard"
In response to many stresses, such as oncogene activation or DNA damage, cells can enter cellular senescence, a state of proliferation arrest accompanied by a senescence-associated secretory phenotype (SASP). Cellular senescence plays a key role in many physiopathological contexts, including cancer, aging and aging-associated diseases, therefore, it is critical to understand how senescence is regulated. Calcium ions (Ca) recently emerged as pivotal regulators of cellular senescence.
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- Cellular senescence leads to a stable halt in cell division and the release of the senescence-associated secretory phenotype (SASP), which includes inflammatory and growth factors that can influence surrounding cells and tissues.
- * The SASP can cause changes in neighboring cells, such as promoting immune responses and contributing to conditions like fibrosis and cancer through a process known as paracrine senescence.
- * New findings reveal that SASP can induce neuroendocrine transdifferentiation (NED) in certain epithelial cancer cells by altering calcium signaling, particularly in older patients with specific tumor characteristics.
Calcium signaling is emerging as a key pathway controlling cellular senescence, a stable cell proliferation arrest playing a fundamental role in pathophysiological conditions, such as embryonic development, wound healing, cancer, and aging. However, how calcium signaling is regulated is still only partially understood. The inositol 1, 4, 5-trisphosphate receptor type 2 (ITPR2), an endoplasmic reticulum calcium release channel, was recently shown to critically contribute to the implementation of senescence, but how ITPR2 expression is controlled is unclear.
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