Cardiac Remodeling and Disease: Current Understanding of STIM1/Orai1-Mediated Store-Operated Ca2+ Entry in Cardiac Function and Pathology

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.

Keywords: Arrhythmias; Cardiac hypertrophy; Cardiomyocytes; Heart; Heart failure; Orai1; STIM1; Store-operated Ca2+ entry.