Calcium ions (Ca2+) and the complex regulatory system governed by Ca2+ signaling have been described to be of crucial importance in numerous aspects related to cell life and death decisions, especially in recent years. The growing attention given to this second messenger is justified by the pleiotropic nature of Ca2+-binding proteins and transporters and their consequent involvement in cell fate decisions. A growing number of works highlight that deregulation of Ca2+ signaling and homoeostasis is often deleterious and drives pathological conditions; in particular, a disruption of the main Ca2+-mediated death mechanisms may lead to uncontrolled cell growth that results in cancer. In this work, we review the latest useful evidence to better understand the complex network of pathways by which Ca2+ regulates cell life and death decisions.

Cell death as a result of calcium signaling modulation: A cancer-centric prospective

Danese A;Leo S;Rimessi A;Wieckowski MR;Fiorica F;Giorgi C;Pinton P.
2021

Abstract

Calcium ions (Ca2+) and the complex regulatory system governed by Ca2+ signaling have been described to be of crucial importance in numerous aspects related to cell life and death decisions, especially in recent years. The growing attention given to this second messenger is justified by the pleiotropic nature of Ca2+-binding proteins and transporters and their consequent involvement in cell fate decisions. A growing number of works highlight that deregulation of Ca2+ signaling and homoeostasis is often deleterious and drives pathological conditions; in particular, a disruption of the main Ca2+-mediated death mechanisms may lead to uncontrolled cell growth that results in cancer. In this work, we review the latest useful evidence to better understand the complex network of pathways by which Ca2+ regulates cell life and death decisions.
Danese, A; Leo, S; Rimessi, A; Wieckowski, Mr; Fiorica, F; Giorgi, C; Pinton, P.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/2476464
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