Abstract
For a long time, Ca2+ entry into cardiomyocytes was considered the sole domain of the L-type Ca2+ channel. Recently, STIM1/Orai1-mediated store-operated Ca2+ entry has been also reported to participate to Ca2+ influx in cardiac cells and has emerged as a key player to alter Ca2+ in the cardiomyocyte. In this review, we will highlight accumulated knowledge about the presence and the potential contribution of STIM1/Orai1-dependent SOCE to cardiac function and its role in the cardiac pathogenesis. Overall, even if STIM1/Orai1 proteins are present in the heart, contradictory results have been reported regarding their contribution to cardiac physiology and pathology, pointing out the necessity of further investigations, a major challenge over the coming years.
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Acknowledgments
We thank Jean-Pierre Benitah and Fabrice Antigny for their careful reading. We thank the Attractivity grant 2014 from the University of Paris-Sud, Agence Nationale de la Recherche (ANR-13-BSV1-0023-01 and ANR-15-CE14-0005), and CORDDIM (Région Ile de France) for their support.
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Bartoli, F., Sabourin, J. (2017). Cardiac Remodeling and Disease: Current Understanding of STIM1/Orai1-Mediated Store-Operated Ca2+ Entry in Cardiac Function and Pathology. In: Groschner, K., Graier, W., Romanin, C. (eds) Store-Operated Ca²⁺ Entry (SOCE) Pathways. Advances in Experimental Medicine and Biology, vol 993. Springer, Cham. https://doi.org/10.1007/978-3-319-57732-6_26
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DOI: https://doi.org/10.1007/978-3-319-57732-6_26
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