Open AccessCardiomyocyte Stim1 Deficiency Exacerbates Doxorubicin Cardiotoxicity by Magnification of Endoplasmic Reticulum Stress
Author(s) -
Jiang Zhu,
Xia Zhang,
Hui Xie,
Yuye Wang,
Xiaoxiao Zhang,
Zhaoheng Lin
Publication year - 2021
Publication title -
journal of inflammation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.656
H-Index - 33
ISSN - 1178-7031
DOI - 10.2147/jir.s304520
Subject(s) - endoplasmic reticulum , stim1 , downregulation and upregulation , apoptosis , orai1 , microbiology and biotechnology , cardiotoxicity , unfolded protein response , gene knockdown , trpc1 , doxorubicin , cancer research , biology , chemistry , medicine , biochemistry , ion channel , receptor , chemotherapy , gene
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.