ArticleJournal of orthopaedic surgery and research2025
MiR-23a-5p affects postmenopausal osteoporosis by targeting ALX3 to regulate osteoblast differentiation.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- From Osteogenesis to Diagnosis: The Role of microRNAs as Biomarkers for Osteoporosis.International journal of molecular sciences · 2026Review
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4 authors.
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Abstract
backgroundPostmenopausal 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.
methodsA 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.
resultsThe 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.
conclusionsmiR-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.
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