Dong S, Liu YQ, Tu YJ, Gao S, Liu YJ, Liu C, Pei ZW. Nicotinamide adenine dinucleotide inhibits the production of reactive oxygen species and myocardial cell pyroptosis caused by hypoxia/re-oxygenation injury. World J Cardiol 2026; 18(1): 114108 [DOI: 10.4330/wjc.v18.i1.114108]
Corresponding Author of This Article
Chang Liu, PhD, Central Laboratory, Central Hospital of Dalian University of Technology, No. 826 Southwest Road, Dalian 116033, Liaoning Province, China. liuch2024@dlut.edu.cn
Research Domain of This Article
Cardiac & Cardiovascular Systems
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Basic Study
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Jan 26, 2026 (publication date) through Jan 15, 2026
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World Journal of Cardiology
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1949-8462
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Dong S, Liu YQ, Tu YJ, Gao S, Liu YJ, Liu C, Pei ZW. Nicotinamide adenine dinucleotide inhibits the production of reactive oxygen species and myocardial cell pyroptosis caused by hypoxia/re-oxygenation injury. World J Cardiol 2026; 18(1): 114108 [DOI: 10.4330/wjc.v18.i1.114108]
World J Cardiol. Jan 26, 2026; 18(1): 114108 Published online Jan 26, 2026. doi: 10.4330/wjc.v18.i1.114108
Nicotinamide adenine dinucleotide inhibits the production of reactive oxygen species and myocardial cell pyroptosis caused by hypoxia/re-oxygenation injury
Shuang Dong, Zuo-Wei Pei, Department of Cardiology, Central Hospital of Dalian University of Technology, Dalian 116033, Liaoning Province, China
Yun-Qi Liu, Shan Gao, Yu-Jie Liu, Chang Liu, Central Laboratory, Central Hospital of Dalian University of Technology, Dalian 116033, Liaoning Province, China
Yi-Jun Tu, Department of Pharmacy, Central Hospital of Dalian University of Technology, Dalian 116033, Liaoning Province, China
Co-first authors: Shuang Dong and Yun-Qi Liu.
Co-corresponding authors: Chang Liu and Zuo-Wei Pei.
Author contributions: Dong S, Liu YQ and Liu C performed the research; Dong S, Liu YQ, Liu C and Pei ZW designed the research study; Tu YJ, Gao S, Liu YJ and Pei ZW analyzed the data; Liu C wrote the manuscript; Dong S and Liu YQ contributed equally to this manuscript and are co-first authors; Liu C and Pei ZW contributed equally to this manuscript and are co-corresponding authors. All authors have read and approved the final manuscript.
Supported by National Natural Science Foundation of China, No. 82303572; Department of Science and Technology of Liaoning Province (China), No. 2024-MS-285; the “Peak Climbing Plan” of Dalian Central Hospital, No. 2023ZZ051; and the Dalian Central Hospital-Initiated Project of “Provincial Key Specialty”, No. 2023SZ015.
Institutional review board statement: This study did not involve human or animal subjects, and thus no ethical approval was required.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: The datasets generated and/or analyzed during the current study are available in the figshare repository (https://10.6084/m9.figshare.28039127).
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Chang Liu, PhD, Central Laboratory, Central Hospital of Dalian University of Technology, No. 826 Southwest Road, Dalian 116033, Liaoning Province, China. liuch2024@dlut.edu.cn
Received: September 15, 2025 Revised: October 11, 2025 Accepted: December 1, 2025 Published online: January 26, 2026 Processing time: 125 Days and 0.7 Hours
Core Tip
Core Tip: Myocardial ischemia/reperfusion (I/R) was a hazardous factor affecting the therapeutic effects of coronary heart disease, especially acute myocardial infarction. The oxidized form of nicotinamide adenine dinucleotide (NAD)-NAD+ is crucial for various cellular functions. This study explored the effects and underlying mechanisms of NAD+ on cell death caused by I/R injury in H9c2 cells. The results showed that supplementing with NAD+ can protect H9c2 cells from pyroptosis induced by I/R injury. Mechanistically, NAD+ supplementation reduces pyroptosis in H9c2 cells triggered by hypoxia/re-oxygenation by inhibiting the activation of the NOD-like receptor pyrin domain-containing 3 inflammasome. These results indicate that NAD+ supplementation could be a promising therapeutic strategy for I/R injury.
