Evidence mapPaperPMID 41239487Full record

ArticleJournal of orthopaedic surgery and research2025

miR-629-3p affects postmenopausal osteoporosis through targeted regulation of BACH1.

Dong Yun, Jinxiang Zhang, Siyuan Ha, Jing Xiao, Caifeng Yan

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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. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

5 authors.

Dong Yun *Yangzhou University, Jiangsu, 225009, China.
Jinxiang Zhang *Department of Joint Surgery and Geriatric Orthopedics, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, 533000, China.
Siyuan HaDepartment of Anesthesiology, The Wuhan Hospital of TCM, Hubei University of Traditional Chinese Medicine, Wuhan, 430014, Hubei, China.
Jing XiaoDepartment of Endocrinology, Wuhan No.9 Hospital, Wuhan, 430000, Hubei, China.
Caifeng YanClinical Medical College of Yangzhou University, No. 88, University South Road, Yangzhou, 225001, China. yancaif2025@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteoporosis (OP) represents a major global health challenge, particularly among postmenopausal women. Currently, there remains a shortage of reliable diagnostic biomarkers and targeted therapies for OP.

methodsA cohort of 254 postmenopausal women (127 OP patients and 127 healthy controls) was analyzed. Serum miR-629-3p levels were measured via qRT-PCR, and diagnostic potential was assessed using ROC analysis. In vitro, MC3T3-E1 osteoblasts were transfected with miR-629-3p mimic/inhibitor and BACH1 overexpression vector (oe-BACH1). Proliferation and apoptosis were evaluated by functional assays (CCK-8, Annexin V-FITC/PI staining), while osteogenic markers (FN1, ITGB1 and RUNX2) were assessed by qPCR. The binding of miR-629-3p to the BACH1 3'UTR was confirmed by luciferase reporter assays.

resultsOur findings revealed significantly decreased miR-629-3p levels in OP patients (P < 0.001), negatively correlating with BACH1 (r = -0.696, P < 0.001) and showing diagnostic potential (AUC = 0.929). Mechanistically, miR-629-3p mimic suppressed BACH1 (P < 0.001), enhancing proliferation, reducing apoptosis, and upregulating RUNX2 (all P < 0.001), while BACH1 overexpression reversed these effects. Luciferase assays confirmed miR-629-3p directly targets BACH1 3'UTR (P < 0.001).

conclusionmiR-629-3p attenuates OP progression by inhibiting BACH1, thereby promoting osteoblast survival, proliferation, and differentiation. Its diagnostic potential and therapeutic role in restoring osteogenic function highlight miR-629-3p/BACH1 as a promising axis for OP management. However, the findings of this study require further validation in animal models to fully establish causality.

Indexed as

Basic-Leucine Zipper Transcription FactorsMicroRNAsOsteoporosis, PostmenopausalAgedAnimalsApoptosisCell ProliferationFemaleHumansMiceMiddle AgedOsteoblastsOsteogenesisBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsMicroRNAsBACH1BiomarkermiR-629-3pOsteoblast functionOsteoporosisRUNX2

Identifiers

PMID41239487
PMCPMC12619170

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.