@Article{biocell.2021.013293,
AUTHOR = {ZHAOHUI HU, XIANGJUN DING, YUYAO JI, XIAOHONG LIU, ZHIWEN DING},
TITLE = {APEX1 protects against oxidative damage-induced cardiomyocyte apoptosis},
JOURNAL = {BIOCELL},
VOLUME = {45},
YEAR = {2021},
NUMBER = {3},
PAGES = {745--749},
URL = {http://www.techscience.com/biocell/v45n3/41677},
ISSN = {1667-5746},
ABSTRACT = {Apurine/pyrimidine-free endonuclease 1 (APEX1) is a multifunctional enzyme that contributes to oxidizationmediated DNA-cleaved base excision repair and redox activation of transcription factors. However, the role of APEX1
during cardiomyocyte oxidative stress injury is not completely understood. In the present study, whether
APEX1 protects oxidative damage-induced cardiomyocytes was investigated. mRNA and protein expression levels of
APEX1 were downregulated in the mouse model of cardiac ischemia-reperfusion injury. Furthermore, the expression
of APEX1 in hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-treated neonatal mice cardiomyocytes was also decreased. APEX1 knockdown
aggravated H<sub>2</sub>O<sub>2</sub>-treated cardiomyocyte apoptosis indexes. By contrast, APEX1 overexpression reversed H<sub>2</sub>O<sub>2</sub>-induced
oxidative damage, as demonstrated by decreased caspase 3 and Bax expression levels. Moreover, homeobox A5
upregulated APEX1. The results of the present study indicated that APEX1 displayed protective effects against oxidative
damage, suggesting that APEX1 may serve as a unique protective strategy for cardiac ischemia-reperfusion injury.},
DOI = {10.32604/biocell.2021.013293}
}