MiR-23a-5p affects postmenopausal osteoporosis by targeting ALX3 to regulate osteoblast differentiation
Abstract Background Postmenopausal women are at an increased risk of developing osteoporosis (OP) due to a decline in estrogen levels. This study focuses on miR-23a-5p as the subject of investigation, aiming to elucidate its expression in postmenopausal osteoporosis (PMOP) and to explore its action...
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BMC
2025-07-01
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| Series: | Journal of Orthopaedic Surgery and Research |
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| Online Access: | https://doi.org/10.1186/s13018-025-06133-z |
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| author | Honghao Zhang Wenjun Rao Rubing Lin Yingxuan Huang |
| author_facet | Honghao Zhang Wenjun Rao Rubing Lin Yingxuan Huang |
| author_sort | Honghao Zhang |
| collection | DOAJ |
| description | Abstract Background Postmenopausal women are at an increased risk of developing osteoporosis (OP) due to a decline in estrogen levels. This study focuses on miR-23a-5p as the subject of investigation, aiming to elucidate its expression in postmenopausal osteoporosis (PMOP) and to explore its action mechanisms. Methods A cohort of 150 postmenopausal women was recruited for this study, encompassing 78 participants diagnosed with OP and 72 controls without OP. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect gene expression levels. OVX rat model was established to simulate clinical features of estrogen deficiency to test the potential role of miR-23a-5p in PMOP. miR-23a-5p overexpression and knockdown MC3T3-E1 cell models were achieved to explore the underlying mechanisms through which miR-23a-5p influence PMOP. Results The expression of miR-23a-5p is upregulated in PMOP and it can distinguish OP patients from non-OP individuals. The expression of miR-23a-5p is related to bone mineral density (BMD) and is a risk factor for PMOP. miR-23a-5p affects serum bone turnover indicators and inhibits osteogenic differentiation marker expression in OVX rats. miR-23a-5p promotes PMOP by negatively regulating the expression of ALX homeobox 3 (ALX3) and affecting the osteogenic differentiation process of MC3T3-E1 cells. Conclusions miR-23a-5p exhibits significantly elevated expression levels in PMOP and it might serve as a promising biomarker. miR-23a-5p plays a pivotal role in the progression of PMOP by negatively regulating ALX3 expression, thereby influencing the osteogenic differentiation process of MC3T3-E1 cells. |
| format | Article |
| id | doaj-art-5cdf9a6850f348bd85ef2b06a2d049a9 |
| institution | Kabale University |
| issn | 1749-799X |
| language | English |
| publishDate | 2025-07-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Orthopaedic Surgery and Research |
| spelling | doaj-art-5cdf9a6850f348bd85ef2b06a2d049a92025-08-20T03:42:56ZengBMCJournal of Orthopaedic Surgery and Research1749-799X2025-07-0120111210.1186/s13018-025-06133-zMiR-23a-5p affects postmenopausal osteoporosis by targeting ALX3 to regulate osteoblast differentiationHonghao Zhang0Wenjun Rao1Rubing Lin2Yingxuan Huang3Department of Special Education and Rehabilitation, Binzhou Medical UniversityDepartment 2 of Orthopedics, People’s Hospital of Yingshan CountyDepartment of Orthopedics, Shenzhen Children’s HospitalGuangxi Key Laboratory for Preclinical and Translational Research on Bone and Joint Degenerative DiseasesAbstract Background Postmenopausal women are at an increased risk of developing osteoporosis (OP) due to a decline in estrogen levels. This study focuses on miR-23a-5p as the subject of investigation, aiming to elucidate its expression in postmenopausal osteoporosis (PMOP) and to explore its action mechanisms. Methods A cohort of 150 postmenopausal women was recruited for this study, encompassing 78 participants diagnosed with OP and 72 controls without OP. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect gene expression levels. OVX rat model was established to simulate clinical features of estrogen deficiency to test the potential role of miR-23a-5p in PMOP. miR-23a-5p overexpression and knockdown MC3T3-E1 cell models were achieved to explore the underlying mechanisms through which miR-23a-5p influence PMOP. Results The expression of miR-23a-5p is upregulated in PMOP and it can distinguish OP patients from non-OP individuals. The expression of miR-23a-5p is related to bone mineral density (BMD) and is a risk factor for PMOP. miR-23a-5p affects serum bone turnover indicators and inhibits osteogenic differentiation marker expression in OVX rats. miR-23a-5p promotes PMOP by negatively regulating the expression of ALX homeobox 3 (ALX3) and affecting the osteogenic differentiation process of MC3T3-E1 cells. Conclusions miR-23a-5p exhibits significantly elevated expression levels in PMOP and it might serve as a promising biomarker. miR-23a-5p plays a pivotal role in the progression of PMOP by negatively regulating ALX3 expression, thereby influencing the osteogenic differentiation process of MC3T3-E1 cells.https://doi.org/10.1186/s13018-025-06133-zPMOPmiR-23a-5pALX3Osteogenic differentiation |
| spellingShingle | Honghao Zhang Wenjun Rao Rubing Lin Yingxuan Huang MiR-23a-5p affects postmenopausal osteoporosis by targeting ALX3 to regulate osteoblast differentiation Journal of Orthopaedic Surgery and Research PMOP miR-23a-5p ALX3 Osteogenic differentiation |
| title | MiR-23a-5p affects postmenopausal osteoporosis by targeting ALX3 to regulate osteoblast differentiation |
| title_full | MiR-23a-5p affects postmenopausal osteoporosis by targeting ALX3 to regulate osteoblast differentiation |
| title_fullStr | MiR-23a-5p affects postmenopausal osteoporosis by targeting ALX3 to regulate osteoblast differentiation |
| title_full_unstemmed | MiR-23a-5p affects postmenopausal osteoporosis by targeting ALX3 to regulate osteoblast differentiation |
| title_short | MiR-23a-5p affects postmenopausal osteoporosis by targeting ALX3 to regulate osteoblast differentiation |
| title_sort | mir 23a 5p affects postmenopausal osteoporosis by targeting alx3 to regulate osteoblast differentiation |
| topic | PMOP miR-23a-5p ALX3 Osteogenic differentiation |
| url | https://doi.org/10.1186/s13018-025-06133-z |
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