Hsa_circ_0020491 promotes polycystic ovary syndrome by interacting with IGF2BP2 through regulation of granular cell autophagy and mitochondrial dysfunction
Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women, yet its underlying mechanisms remain incompletely understood. This study investigated the role of hsa_circ_0020491 in PCOS pathogenesis, focusing on granulosa cells (GCs). Analysis of GCs from PCOS patients and controls rev...
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| Language: | English |
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Taylor & Francis Group
2025-12-01
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| Series: | Gynecological Endocrinology |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/09513590.2025.2536579 |
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| author | XiaLing Huang Fen Yu |
| author_facet | XiaLing Huang Fen Yu |
| author_sort | XiaLing Huang |
| collection | DOAJ |
| description | Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women, yet its underlying mechanisms remain incompletely understood. This study investigated the role of hsa_circ_0020491 in PCOS pathogenesis, focusing on granulosa cells (GCs). Analysis of GCs from PCOS patients and controls revealed significant upregulation of both hsa_circ_0020491 and IGF2BP2, with their expression levels positively correlated. In a dihydrotestosterone (DHT)-treated KGN cell model of PCOS, silencing either circ_0020491 or IGF2BP2 mitigated autophagy dysregulation and mitochondrial dysfunction, evidenced by altered autophagy-related proteins, mitochondrial membrane potential, ATP levels, mtDNA content, and reactive oxygen species. Mechanistically, circ_0020491 binds to and stabilizes IGF2BP2, amplifying its effects. Overexpression of IGF2BP2 counteracted the improvements induced by circ_0020491 knockdown. In vivo, a dehydroepiandrosterone (DHEA)-induced PCOS mouse model confirmed that circ_0020491 suppression attenuated disease progression, improved mitochondrial function, and reduced excessive autophagy. These findings demonstrate that hsa_circ_0020491 exacerbates PCOS by interacting with IGF2BP2 to disrupt autophagy and mitochondrial homeostasis in GCs, offering a potential therapeutic target. |
| format | Article |
| id | doaj-art-deaed054c400403e8985550903878024 |
| institution | DOAJ |
| issn | 0951-3590 1473-0766 |
| language | English |
| publishDate | 2025-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Gynecological Endocrinology |
| spelling | doaj-art-deaed054c400403e89855509038780242025-08-20T02:46:24ZengTaylor & Francis GroupGynecological Endocrinology0951-35901473-07662025-12-0141110.1080/09513590.2025.2536579Hsa_circ_0020491 promotes polycystic ovary syndrome by interacting with IGF2BP2 through regulation of granular cell autophagy and mitochondrial dysfunctionXiaLing Huang0Fen Yu1Department Of gynecology, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan City, Hubei Province, ChinaDepartment Of gynecology, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan City, Hubei Province, ChinaPolycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women, yet its underlying mechanisms remain incompletely understood. This study investigated the role of hsa_circ_0020491 in PCOS pathogenesis, focusing on granulosa cells (GCs). Analysis of GCs from PCOS patients and controls revealed significant upregulation of both hsa_circ_0020491 and IGF2BP2, with their expression levels positively correlated. In a dihydrotestosterone (DHT)-treated KGN cell model of PCOS, silencing either circ_0020491 or IGF2BP2 mitigated autophagy dysregulation and mitochondrial dysfunction, evidenced by altered autophagy-related proteins, mitochondrial membrane potential, ATP levels, mtDNA content, and reactive oxygen species. Mechanistically, circ_0020491 binds to and stabilizes IGF2BP2, amplifying its effects. Overexpression of IGF2BP2 counteracted the improvements induced by circ_0020491 knockdown. In vivo, a dehydroepiandrosterone (DHEA)-induced PCOS mouse model confirmed that circ_0020491 suppression attenuated disease progression, improved mitochondrial function, and reduced excessive autophagy. These findings demonstrate that hsa_circ_0020491 exacerbates PCOS by interacting with IGF2BP2 to disrupt autophagy and mitochondrial homeostasis in GCs, offering a potential therapeutic target.https://www.tandfonline.com/doi/10.1080/09513590.2025.2536579Polycystic ovary syndromehsa_circ_0020491IGF2BP2granular cellsautophagymitochondria |
| spellingShingle | XiaLing Huang Fen Yu Hsa_circ_0020491 promotes polycystic ovary syndrome by interacting with IGF2BP2 through regulation of granular cell autophagy and mitochondrial dysfunction Gynecological Endocrinology Polycystic ovary syndrome hsa_circ_0020491 IGF2BP2 granular cells autophagy mitochondria |
| title | Hsa_circ_0020491 promotes polycystic ovary syndrome by interacting with IGF2BP2 through regulation of granular cell autophagy and mitochondrial dysfunction |
| title_full | Hsa_circ_0020491 promotes polycystic ovary syndrome by interacting with IGF2BP2 through regulation of granular cell autophagy and mitochondrial dysfunction |
| title_fullStr | Hsa_circ_0020491 promotes polycystic ovary syndrome by interacting with IGF2BP2 through regulation of granular cell autophagy and mitochondrial dysfunction |
| title_full_unstemmed | Hsa_circ_0020491 promotes polycystic ovary syndrome by interacting with IGF2BP2 through regulation of granular cell autophagy and mitochondrial dysfunction |
| title_short | Hsa_circ_0020491 promotes polycystic ovary syndrome by interacting with IGF2BP2 through regulation of granular cell autophagy and mitochondrial dysfunction |
| title_sort | hsa circ 0020491 promotes polycystic ovary syndrome by interacting with igf2bp2 through regulation of granular cell autophagy and mitochondrial dysfunction |
| topic | Polycystic ovary syndrome hsa_circ_0020491 IGF2BP2 granular cells autophagy mitochondria |
| url | https://www.tandfonline.com/doi/10.1080/09513590.2025.2536579 |
| work_keys_str_mv | AT xialinghuang hsacirc0020491promotespolycysticovarysyndromebyinteractingwithigf2bp2throughregulationofgranularcellautophagyandmitochondrialdysfunction AT fenyu hsacirc0020491promotespolycysticovarysyndromebyinteractingwithigf2bp2throughregulationofgranularcellautophagyandmitochondrialdysfunction |