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World J Cardiol. Oct 26, 2026; 18(10): 125900
Published online Oct 26, 2026. doi: 10.4330/wjc.125900
Published online Oct 26, 2026. doi: 10.4330/wjc.125900
Excessive mitochondrial fission in myocardial ischemia/reperfusion injury: Pathophysiological relevance and potential cardioprotective modulation by plant-derived interventions and electroacupuncture
Li Sun, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China; First Teaching Hospital of Tianjin University of Traditional Chinese Medicine/National Clinical Research Center for Chinese Medicine, Tianjin 300380, China
Xing-Yi Sun, Zi-Han Na, Lin Li, Tian-Yu Cao, Xin-Ran Li, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
Yi-Jia Liu, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300250, China
Ya-Dong Fan, School of Traditional Chinese Medicine, Faculty of Medicine, Yangzhou University, Yangzhou 225009, Jiangsu Province, China
Gui-Ping Hu, School of Engineering Medicine, Beihang University, Beijing 100191, China
Shuo Wang, State Key Laboratory of Chinese Medicine Modernization, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
Co-first authors: Li Sun and Xing-Yi Sun.
Co-corresponding authors: Gui-Ping Hu and Shuo Wang.
Author contributions: Sun L and Sun XY contributed to the literature search and screening, and the drafting and revision of the manuscript; Sun L contributed to the design and preparation of the figures and tables; Sun XY contributed to the extraction and curation of the data presented in the evidence tables; Na ZH contributed to the preparation of the Supplementary materials; Liu YJ, Cao TY and Li XR contributed to the cross-check of the extracted information and Supplementary materials; Li L, Hu GP, Wang S and Fan YD contributed to the funding acquisition; Fan YD and Wang S contributed to the critical revision; Hu GP contributed to the review and editing of the manuscript; Wang S contributed to the conception and supervision of the study. Hu GP and Wang S contributed equally to this work as co-corresponding authors. Sun L and Sun XY contributed equally to this work as co-first authors.
AI contribution statement: The authors declare that no AI tools were used in the development or writing of this manuscript and take full responsibility for its integrity, accuracy, and originality.
Supported by the National Natural Science Foundation of China, No. 82104565 and No. 82405328; the Research Project of the Tianjin Municipal Education Commission, No. 2023KJ144; the Young Scholar Fund Project of the State Key Laboratory of Component-Based Chinese Medicine, No. QMJJ202403; and the Open Research Project of the State Key Laboratory of Component-Based Chinese Medicine, No. CBCM2024202.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Shuo Wang, MD, State Key Laboratory of Chinese Medicine Modernization, Tianjin University of Traditional Chinese Medicine, West District, Tuanbo New City, Jinghai District, Tianjin 301617, China. wssean1609@163.com
Received: July 21, 2026
Revised: September 9, 2026
Accepted: October 20, 2026
Published online: October 26, 2026
Processing time: 94 Days and 22.2 Hours
Revised: September 9, 2026
Accepted: October 20, 2026
Published online: October 26, 2026
Processing time: 94 Days and 22.2 Hours
Core Tip
Core Tip: Excessive mitochondrial fission is not merely a morphological consequence of myocardial ischemia/reperfusion injury, but a potential amplifier of mitochondrial dysfunction and cardiomyocyte death. This review highlights the complementary contributions of dynamin-related protein 1-centered fission activation and impaired fusion-mediated network repair. It further emphasizes that broad mitochondrial protection should not be equated with direct modulation of the fusion-fission machinery. Plant-derived interventions and electroacupuncture show experimental promise, but mechanistic causality and translational relevance remain insufficiently established.