Exercise preconditioning inhibits doxorubicin-induced cardiotoxicity via YAP/STAT3 signaling
© 2024 The Authors..
Doxorubicin (DOX) possesses strong anti-tumor effects but is limited by its irreversible cardiac toxicity. The relationship between exercise, a known enhancer of cardiovascular health, and DOX-induced cardiotoxicity has been a focus of recent research. Exercise has been suggested to mitigate DOX's cardiac harm by modulating the Yes-associated protein (YAP) and Signal transducer and activator of transcription 3 (STAT3) pathways, which are crucial in regulating cardiac cell functions and responses to damage. This study aimed to assess the protective role of exercise preconditioning against DOX-induced cardiac injury. We used Sprague-Dawley rats, divided into five groups (control, DOX, exercise preconditioning (EP), EP-DOX, and verteporfin + EP + DOX), to investigate the potential mechanisms. Our findings, including echocardiography, histological staining, Western blot, and q-PCR analysis, demonstrated that exercise preconditioning could alleviate DOX-induced cardiac dysfunction and structural damage. Notably, exercise preconditioning enhanced the nuclear localization and co-localization of YAP and STAT3. Our study suggests that exercise preconditioning may counteract DOX-induced cardiotoxicity by activating the YAP/STAT3 pathway, highlighting a potential therapeutic approach for reducing DOX's cardiac side effects.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:10 |
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Enthalten in: |
Heliyon - 10(2024), 6 vom: 30. März, Seite e27035 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Wang, Chuan-Zhi [VerfasserIn] |
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Links: |
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Themen: |
Cardiac protection |
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Anmerkungen: |
Date Revised 23.03.2024 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
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doi: |
10.1016/j.heliyon.2024.e27035 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM370052501 |
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520 | |a Doxorubicin (DOX) possesses strong anti-tumor effects but is limited by its irreversible cardiac toxicity. The relationship between exercise, a known enhancer of cardiovascular health, and DOX-induced cardiotoxicity has been a focus of recent research. Exercise has been suggested to mitigate DOX's cardiac harm by modulating the Yes-associated protein (YAP) and Signal transducer and activator of transcription 3 (STAT3) pathways, which are crucial in regulating cardiac cell functions and responses to damage. This study aimed to assess the protective role of exercise preconditioning against DOX-induced cardiac injury. We used Sprague-Dawley rats, divided into five groups (control, DOX, exercise preconditioning (EP), EP-DOX, and verteporfin + EP + DOX), to investigate the potential mechanisms. Our findings, including echocardiography, histological staining, Western blot, and q-PCR analysis, demonstrated that exercise preconditioning could alleviate DOX-induced cardiac dysfunction and structural damage. Notably, exercise preconditioning enhanced the nuclear localization and co-localization of YAP and STAT3. Our study suggests that exercise preconditioning may counteract DOX-induced cardiotoxicity by activating the YAP/STAT3 pathway, highlighting a potential therapeutic approach for reducing DOX's cardiac side effects | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Cardiac protection | |
650 | 4 | |a Cardiotoxicity | |
650 | 4 | |a Doxorubicin | |
650 | 4 | |a Exercise preconditioning | |
650 | 4 | |a STAT3 | |
650 | 4 | |a YAP | |
700 | 1 | |a Guo, Heng-Zhi |e verfasserin |4 aut | |
700 | 1 | |a Leng, Jing-Zhi |e verfasserin |4 aut | |
700 | 1 | |a Liang, Zhi-De |e verfasserin |4 aut | |
700 | 1 | |a Wang, Jing-Tai |e verfasserin |4 aut | |
700 | 1 | |a Luo, Li-Jie |e verfasserin |4 aut | |
700 | 1 | |a Wang, Shi-Qiang |e verfasserin |4 aut | |
700 | 1 | |a Yuan, Yang |e verfasserin |4 aut | |
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