Open Access

ARTICLE

APEX1 protects against oxidative damage-induced cardiomyocyte apoptosis

ZHAOHUI HU^1,2, XIANGJUN DING³, YUYAO JI², XIAOHONG LIU^4,*, ZHIWEN DING^2,*

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, ; Zhiwen Ding,

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

Received 01 August 2020; Accepted 23 October 2020; Issue published 03 March 2021

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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