Epimedin C enhances mitochondrial energy supply by regulating the interaction between MIC25 and UBC in rodent model.
The study investigates the molecular mechanisms underlying the skeletal muscle-enhancing effects of Epimedin C, a natural flavonoid, focusing on its interaction with the mitochondrial cristae structural protein MIC25. Using C57BL/6 mice, we demonstrate that Epimedin C enhances exercise performance t...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2025-01-01
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| Series: | PLoS ONE |
| Online Access: | https://doi.org/10.1371/journal.pone.0325031 |
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| author | Mi Huang Lei Yu Zhong Li Ying Wang Chunlin Yang |
| author_facet | Mi Huang Lei Yu Zhong Li Ying Wang Chunlin Yang |
| author_sort | Mi Huang |
| collection | DOAJ |
| description | The study investigates the molecular mechanisms underlying the skeletal muscle-enhancing effects of Epimedin C, a natural flavonoid, focusing on its interaction with the mitochondrial cristae structural protein MIC25. Using C57BL/6 mice, we demonstrate that Epimedin C enhances exercise performance through preservation of mitochondrial function. Proteomic analysis identified MIC25 as a key protein modulated by Epimedin C, whose stability is regulated via ubiquitin-dependent degradation. Functional experiments revealed that Epimedin C disrupts the interaction between MIC25 and ubiquitin-conjugating enzyme C (UBC), preventing MIC25 degradation and maintaining the integrity of the mitochondrial contact site and cristae organizing system (MICOS). This stabilization preserves mitochondrial cristae structure, improves ATP production, and delays muscle fatigue. Notably, MIC25 overexpression mimicked Epimedin C's effects, while its knockdown abolished these benefits. Our findings establish MIC25 as a critical effector of Epimedin C, elucidating a novel pathway through which flavonoids maintain mitochondrial homeostasis to enhance muscle function. These insights hold promise for developing therapies targeting muscle atrophy and metabolic disorders. |
| format | Article |
| id | doaj-art-83e4d9e4b3274a5e91480b1da384bfd6 |
| institution | Kabale University |
| issn | 1932-6203 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-83e4d9e4b3274a5e91480b1da384bfd62025-08-20T03:47:07ZengPublic Library of Science (PLoS)PLoS ONE1932-62032025-01-01205e032503110.1371/journal.pone.0325031Epimedin C enhances mitochondrial energy supply by regulating the interaction between MIC25 and UBC in rodent model.Mi HuangLei YuZhong LiYing WangChunlin YangThe study investigates the molecular mechanisms underlying the skeletal muscle-enhancing effects of Epimedin C, a natural flavonoid, focusing on its interaction with the mitochondrial cristae structural protein MIC25. Using C57BL/6 mice, we demonstrate that Epimedin C enhances exercise performance through preservation of mitochondrial function. Proteomic analysis identified MIC25 as a key protein modulated by Epimedin C, whose stability is regulated via ubiquitin-dependent degradation. Functional experiments revealed that Epimedin C disrupts the interaction between MIC25 and ubiquitin-conjugating enzyme C (UBC), preventing MIC25 degradation and maintaining the integrity of the mitochondrial contact site and cristae organizing system (MICOS). This stabilization preserves mitochondrial cristae structure, improves ATP production, and delays muscle fatigue. Notably, MIC25 overexpression mimicked Epimedin C's effects, while its knockdown abolished these benefits. Our findings establish MIC25 as a critical effector of Epimedin C, elucidating a novel pathway through which flavonoids maintain mitochondrial homeostasis to enhance muscle function. These insights hold promise for developing therapies targeting muscle atrophy and metabolic disorders.https://doi.org/10.1371/journal.pone.0325031 |
| spellingShingle | Mi Huang Lei Yu Zhong Li Ying Wang Chunlin Yang Epimedin C enhances mitochondrial energy supply by regulating the interaction between MIC25 and UBC in rodent model. PLoS ONE |
| title | Epimedin C enhances mitochondrial energy supply by regulating the interaction between MIC25 and UBC in rodent model. |
| title_full | Epimedin C enhances mitochondrial energy supply by regulating the interaction between MIC25 and UBC in rodent model. |
| title_fullStr | Epimedin C enhances mitochondrial energy supply by regulating the interaction between MIC25 and UBC in rodent model. |
| title_full_unstemmed | Epimedin C enhances mitochondrial energy supply by regulating the interaction between MIC25 and UBC in rodent model. |
| title_short | Epimedin C enhances mitochondrial energy supply by regulating the interaction between MIC25 and UBC in rodent model. |
| title_sort | epimedin c enhances mitochondrial energy supply by regulating the interaction between mic25 and ubc in rodent model |
| url | https://doi.org/10.1371/journal.pone.0325031 |
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