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APEX1 protects against oxidative damage-induced cardiomyocyte apoptosis

ZHAOHUI HU1,2, XIANGJUN DING3, YUYAO JI2, XIAOHONG LIU4,*, ZHIWEN DING2,*

1 Department of Cardiology, Tongji University Affiliated Tongji Hospital, Shanghai, 200065, China
2 Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, 200032, China
3 The West Coast New Area of Qingdao Traditional Chinese Medicine Hospital, Qingdao, 266500, China
4 Cardiovascular Department of Internal Medicine, Central Hospital of Karamay, Karamay, 834000, China

* Address correspondence to: Xiaohong Liu, email; Zhiwen Ding, email

BIOCELL 2021, 45(3), 745-749. https://doi.org/10.32604/biocell.2021.013293

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 (H2O2)-treated neonatal mice cardiomyocytes was also decreased. APEX1 knockdown aggravated H2O2-treated cardiomyocyte apoptosis indexes. By contrast, APEX1 overexpression reversed H2O2-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.

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HU, Z., DING, X., JI, Y., LIU, X., DING, Z. (2021). APEX1 protects against oxidative damage-induced cardiomyocyte apoptosis. BIOCELL, 45(3), 745–749. https://doi.org/10.32604/biocell.2021.013293

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cc This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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