miR-208a-3p discriminates osteoporosis, predicts fracture, and regulates osteoclast activation through targeting STC1
Abstract Background Osteoporosis (OP) frequently occurs in post-menopausal women, increasing the risk of fracture. Early screening OP could improve the prevention of fractures.This study focused on the significance of miR-208a-3p in diagnosing OP and development regulation, aiming to explore a novel...
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2025-01-01
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Online Access: | https://doi.org/10.1186/s13018-025-05512-w |
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author | Hongbing Qian Fei Jia Huiling Qin |
author_facet | Hongbing Qian Fei Jia Huiling Qin |
author_sort | Hongbing Qian |
collection | DOAJ |
description | Abstract Background Osteoporosis (OP) frequently occurs in post-menopausal women, increasing the risk of fracture. Early screening OP could improve the prevention of fractures.This study focused on the significance of miR-208a-3p in diagnosing OP and development regulation, aiming to explore a novel biomarker and therapeutic target for OP. Methods The study enrolled a total of 154 post-menopausal women and grouping was performed based on the incidence of OP and fracture. The significance of miR-208a-3p was evaluated from the perspectives of menopausal correlation, OP diagnosis, and fracture prediction. In mechanism, the regulatory effect and mechanism of miR-208a-3p on osteoclast activation was investigated. Results miR-208a-3p was menopause-related showing a negative correlation with E2 and positive correlations with FSH and LH. Significant upregulation of miR-208a-3p was observed in post-menopausal women with OP and showed significant diagnostic potential. Increasing miR-208a-3p was positively correlated with bone metabolism markers and negatively correlated with BMD of post-menopausal women with OP. Moreover, miR-208a-3p was also identified as a risk factor for fracture. STC1 was identified as a direct target of miR-208a-3p and was negatively regulated by miR-208a-3p. Silencing miR-208a-3p significantly alleviated macrophage inflammation and osteoblast activation, which was reversed by the knockdown of STC1. Conclusion Serum miR-208a-3p served as a diagnostic biomarker for OP and a risk factor for fracture in post-menopausal women. miR-208a-3p regulated macrophage inflammation and further mediated osteoclast activation via targeting STC1. |
format | Article |
id | doaj-art-935dbc62acc94d15977001a789f665f5 |
institution | Kabale University |
issn | 1749-799X |
language | English |
publishDate | 2025-01-01 |
publisher | BMC |
record_format | Article |
series | Journal of Orthopaedic Surgery and Research |
spelling | doaj-art-935dbc62acc94d15977001a789f665f52025-02-02T12:34:18ZengBMCJournal of Orthopaedic Surgery and Research1749-799X2025-01-0120111010.1186/s13018-025-05512-wmiR-208a-3p discriminates osteoporosis, predicts fracture, and regulates osteoclast activation through targeting STC1Hongbing Qian0Fei Jia1Huiling Qin2Spine Surgery, Kunshan Hospital of Traditional Chinese MedicineDepartment of Spine Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityDepartment of Rehabilitation, The Affiliated Hospital of Youjiang Medical University for NationalitiesAbstract Background Osteoporosis (OP) frequently occurs in post-menopausal women, increasing the risk of fracture. Early screening OP could improve the prevention of fractures.This study focused on the significance of miR-208a-3p in diagnosing OP and development regulation, aiming to explore a novel biomarker and therapeutic target for OP. Methods The study enrolled a total of 154 post-menopausal women and grouping was performed based on the incidence of OP and fracture. The significance of miR-208a-3p was evaluated from the perspectives of menopausal correlation, OP diagnosis, and fracture prediction. In mechanism, the regulatory effect and mechanism of miR-208a-3p on osteoclast activation was investigated. Results miR-208a-3p was menopause-related showing a negative correlation with E2 and positive correlations with FSH and LH. Significant upregulation of miR-208a-3p was observed in post-menopausal women with OP and showed significant diagnostic potential. Increasing miR-208a-3p was positively correlated with bone metabolism markers and negatively correlated with BMD of post-menopausal women with OP. Moreover, miR-208a-3p was also identified as a risk factor for fracture. STC1 was identified as a direct target of miR-208a-3p and was negatively regulated by miR-208a-3p. Silencing miR-208a-3p significantly alleviated macrophage inflammation and osteoblast activation, which was reversed by the knockdown of STC1. Conclusion Serum miR-208a-3p served as a diagnostic biomarker for OP and a risk factor for fracture in post-menopausal women. miR-208a-3p regulated macrophage inflammation and further mediated osteoclast activation via targeting STC1.https://doi.org/10.1186/s13018-025-05512-wMenopausal osteoporosisOsteoclast differentiationEarly detectionFracture |
spellingShingle | Hongbing Qian Fei Jia Huiling Qin miR-208a-3p discriminates osteoporosis, predicts fracture, and regulates osteoclast activation through targeting STC1 Journal of Orthopaedic Surgery and Research Menopausal osteoporosis Osteoclast differentiation Early detection Fracture |
title | miR-208a-3p discriminates osteoporosis, predicts fracture, and regulates osteoclast activation through targeting STC1 |
title_full | miR-208a-3p discriminates osteoporosis, predicts fracture, and regulates osteoclast activation through targeting STC1 |
title_fullStr | miR-208a-3p discriminates osteoporosis, predicts fracture, and regulates osteoclast activation through targeting STC1 |
title_full_unstemmed | miR-208a-3p discriminates osteoporosis, predicts fracture, and regulates osteoclast activation through targeting STC1 |
title_short | miR-208a-3p discriminates osteoporosis, predicts fracture, and regulates osteoclast activation through targeting STC1 |
title_sort | mir 208a 3p discriminates osteoporosis predicts fracture and regulates osteoclast activation through targeting stc1 |
topic | Menopausal osteoporosis Osteoclast differentiation Early detection Fracture |
url | https://doi.org/10.1186/s13018-025-05512-w |
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