Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathway

Abstract Myocardial cold ischemia/reperfusion (I/R) injury is an inevitable consequence of heart transplantation, significantly affecting survival rates and therapeutic outcomes. Growth Differentiation Factor 15 (GDF15) has been shown to regulate GPX4-mediated ferroptosis, playing a critical role in...

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Main Authors: Yuxi Zhang, Junbiao Zhan, Zhen Qiu, Hao Tian, Shaoqing Lei, Qin Huang, Rui Xue, Qian Sun, Zhongyuan Xia
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-00112-4
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author Yuxi Zhang
Junbiao Zhan
Zhen Qiu
Hao Tian
Shaoqing Lei
Qin Huang
Rui Xue
Qian Sun
Zhongyuan Xia
author_facet Yuxi Zhang
Junbiao Zhan
Zhen Qiu
Hao Tian
Shaoqing Lei
Qin Huang
Rui Xue
Qian Sun
Zhongyuan Xia
author_sort Yuxi Zhang
collection DOAJ
description Abstract Myocardial cold ischemia/reperfusion (I/R) injury is an inevitable consequence of heart transplantation, significantly affecting survival rates and therapeutic outcomes. Growth Differentiation Factor 15 (GDF15) has been shown to regulate GPX4-mediated ferroptosis, playing a critical role in mitigating I/R injury. Meanwhile, verbascoside (VB), an active compound extracted from the herbaceous plant, has demonstrated myocardial protective effects. In this study, heart transplantation was performed using a modified non-suture cuff technique, with VB administered at a dose of 20 mg/kg/day via intraperitoneal injection for 3 days in vivo. In vitro, cardiomyocytes were pretreated with 50 µg/ml VB for 24 h. VB treatment significantly reduced histopathological injury, decreased myocardial injury markers, and inhibited ferroptosis and oxidative stress during myocardial cold I/R injury in vivo. In vitro experiments further demonstrated that GDF15 alleviates ferroptosis induced by hypoxic reoxygenation by upregulating GPX4. Therefore, it is concluded that VB preconditioning can effectively reduce ferroptosis induced by myocardial cold I/R after heterotopic heart transplantation, possibly through up-regulation of GDF15/GPX4/SLC7A11 pathway.
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spelling doaj-art-4967e28cd0bc43d69b1edf187db9a81e2025-08-20T03:09:20ZengNature PortfolioScientific Reports2045-23222025-05-0115111410.1038/s41598-025-00112-4Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathwayYuxi Zhang0Junbiao Zhan1Zhen Qiu2Hao Tian3Shaoqing Lei4Qin Huang5Rui Xue6Qian Sun7Zhongyuan Xia8Department of Anesthesiology, Wuhan University, Renmin HospitalDepartment of Anesthesiology, Wuhan University, Renmin HospitalDepartment of Anesthesiology, Wuhan University, Renmin HospitalDepartment of Anesthesiology, Wuhan University, Renmin HospitalDepartment of Anesthesiology, Wuhan University, Renmin HospitalDepartment of Anesthesiology, Wuhan University, Renmin HospitalDepartment of Anesthesiology, Hubei University of Medicine, Renmin HospitalDepartment of Anesthesiology, Wuhan University, Renmin HospitalDepartment of Anesthesiology, Wuhan University, Renmin HospitalAbstract Myocardial cold ischemia/reperfusion (I/R) injury is an inevitable consequence of heart transplantation, significantly affecting survival rates and therapeutic outcomes. Growth Differentiation Factor 15 (GDF15) has been shown to regulate GPX4-mediated ferroptosis, playing a critical role in mitigating I/R injury. Meanwhile, verbascoside (VB), an active compound extracted from the herbaceous plant, has demonstrated myocardial protective effects. In this study, heart transplantation was performed using a modified non-suture cuff technique, with VB administered at a dose of 20 mg/kg/day via intraperitoneal injection for 3 days in vivo. In vitro, cardiomyocytes were pretreated with 50 µg/ml VB for 24 h. VB treatment significantly reduced histopathological injury, decreased myocardial injury markers, and inhibited ferroptosis and oxidative stress during myocardial cold I/R injury in vivo. In vitro experiments further demonstrated that GDF15 alleviates ferroptosis induced by hypoxic reoxygenation by upregulating GPX4. Therefore, it is concluded that VB preconditioning can effectively reduce ferroptosis induced by myocardial cold I/R after heterotopic heart transplantation, possibly through up-regulation of GDF15/GPX4/SLC7A11 pathway.https://doi.org/10.1038/s41598-025-00112-4VerbascosideHeart transplantationMyocardial cold ischemia /reperfusion injuryFerroptosisGDF15
spellingShingle Yuxi Zhang
Junbiao Zhan
Zhen Qiu
Hao Tian
Shaoqing Lei
Qin Huang
Rui Xue
Qian Sun
Zhongyuan Xia
Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathway
Scientific Reports
Verbascoside
Heart transplantation
Myocardial cold ischemia /reperfusion injury
Ferroptosis
GDF15
title Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathway
title_full Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathway
title_fullStr Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathway
title_full_unstemmed Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathway
title_short Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathway
title_sort verbascoside attenuates myocardial ischemia reperfusion induced ferroptosis following heterotopic heart transplantation via modulating gdf15 gpx4 slc7a11 pathway
topic Verbascoside
Heart transplantation
Myocardial cold ischemia /reperfusion injury
Ferroptosis
GDF15
url https://doi.org/10.1038/s41598-025-00112-4
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