ORIGINAL RESEARCH article
Front. Cell Dev. Biol.
Sec. Cell Death and Survival
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1605513
This article is part of the Research TopicMechanisms and Therapeutic Strategies in Cellular Injury and RepairView all articles
Morinda officinalis oligosaccharides attenuate mitochondria-associated ferroptosis via the NOX4/mitoGPX4 pathway in Myocardial Ischemia-Reperfusion Injury
Provisionally accepted
Yuqiong Chen1*
Yuan Tian2
Bo Guan1Yiling Chang3Xiaopei Yan1Qi Song1Wenting Chen1Lin Chen1Wei Li1Wenjun Mao1Yan Zhang4*Chao Chen1*Su Li5*- 1Suzhou Municipal Hospital, Suzhou, China
- 2Jinshan Hospital, Fudan University, Shanghai, Shanghai Municipality, China
- 3Jiangsu Taizhou People's Hospital, Taizhou, Jiangsu Province, China
- 4Xuzhou Central Hospital, Xuzhou, Jiangsu Province, China
- 5Zhongshan Hospital, Fudan University, Shanghai, Shanghai Municipality, China
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Aim: To explore the benefits of Morinda officinalis oligosaccharides (MOO) on ischemiareperfusion (I/R) injury and the possible mechanisms involved.: Myocardial I/R injury were induced by left anterior descending branch ligation. MOO pretreatment was given orally 2 weeks prior to ischemic treatment. Echocardiograms, biochemical parameters, and histological and immunohistochemical analyses were used to determine the benefits of MOO on myocardial I/R injury. Oxidative stress and ferroptosis were examined by biochemical parameters, western blot, immunohistochemistry, and Tunel staining. Results: MOO improved cardiac function and reduced myocardial oxidative stress and ferroptosis, which was associated with the inhibition of NADPH Oxidase 4 (NOX4) expression. Whereas, the upregulation of NOX4 abolished the benefits of MOO. Furthermore, MOO enhanced mitochondrial superoxide dismutase 2 (SOD2) activity and stimulated the mitochondrial translocation of glutathione peroxidase 4 (mitoGPX4) by inhibiting NOX4. Mitochondria-specific GPX4 overexpression attenuated mitochondrial oxidative stress and suppressed mitochondria-associated ferroptosis in cardiomyocytes that suffered from hypoxia-reoxygenation (H/R) injury, even after NOX4 overexpression. Conclusion: These results indicate the beneficial effects of MOO on myocardial I/R injury by suppressing oxidative stress and mitochondria-associated ferroptosis through NOX4/mitoGPX4 pathway.
Keywords: Morinda officinalis Oligosaccharides, Myocardial ischemia-reperfusion injury, NOX4, GPx4, ferroptosis
Received: 03 Apr 2025; Accepted: 06 May 2025.
Copyright: © 2025 Chen, Tian, Guan, Chang, Yan, Song, Chen, Chen, Li, Mao, Zhang, Chen and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Yuqiong Chen, Suzhou Municipal Hospital, Suzhou, China
Yan Zhang, Xuzhou Central Hospital, Xuzhou, 221000, Jiangsu Province, China
Chao Chen, Suzhou Municipal Hospital, Suzhou, China
Su Li, Zhongshan Hospital, Fudan University, Shanghai, 200032, Shanghai Municipality, China
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