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Doxorubicin (Dox) is an effective anticancer agent; however, its cardiotoxicity remains a challenge. Dysfunction of intracellular calcium ion (Ca 2+ ) is implicated in the process of Dox-induced cardiomyocyte apoptosis. Although store-operated Ca 2+ entry (SOCE) is suggested to be responsible for Ca 2+ entry in cardiomyocytes, the direct role of store-operated Ca 2+ channels in Dox-related cardiomyocyte apoptosis is unknown.

Cardiomyocyte Stim1 Deficiency Exacerbates Doxorubicin Cardiotoxicity by Magnification of Endoplasmic Reticulum Stress