ArticleCommunications biology2023
LncRNA SNHG14 activates autophagy via regulating miR-493-5p/Mef2c axis to alleviate osteoporosis progression.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Long Non-Coding RNAsCurrent issues in molecular biology · 2026Article
- The crosstalk network of non-coding RNAs: Emerging opportunities for the clinical application of osteoporosis.Non-coding RNA research · 2026Review
- The DNA Methylation-Autophagy Axis: A Driver of MSC Fate Imbalance in Skeletal Aging and Osteoporosis.Biology · 2026Review
- Screening and validation of autophagy-related mRNAs and lncRNAs in bone nonunion based on transcriptome sequencing analysis.Human cell · 2025Article
- The role of non-coding RNA regulates stem cell programmed death in disease therapy.Non-coding RNA research · 2025Review
- LncRNA CTD-2555A7.2 promotes bone formation with LncRNA-specific cascade amplification strategy.Scientific reports · 2025Article
- LINC00968 accelerates osteogenic differentiation of bone marrow mesenchymal stem cells via the miR-17-5p/STAT3 axis.Journal of orthopaedic surgery and research · 2025Article
- Non-coding RNAs mediate mechanical load-regulating bone metabolic homeostasis.Frontiers in cell and developmental biology · 2025Review
- LncRNA MAGI2-AS3 promotes fracture healing through downregulation of miR-223-3p.Journal of orthopaedic surgery and research · 2024Article
- Exploration and bioinformatic prediction for profile of mRNA bound to circular RNA BTBD7_hsa_circ_0000563 in coronary artery disease.BMC cardiovascular disorders · 2024Article
- Early diagnosis value of lncRNA SNHG14 combined with miR-493-5p in gestational diabetes mellitus and its correlation with pregnancy outcome.Diabetes & vascular disease researchArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis is a progressive bone disease caused by impaired function of endogenous bone marrow-derived mesenchymal stem cells (BMSCs). Herein, we investigated the mechanism of lncRNA SNHG14 in osteoporosis progression. BMSCs were isolated from BALB/c mice. The osteogenic ability of BMSCs was assessed by Alkaline phosphatase (ALP) and Alizarin Red S Staining (ARS) staining. The interaction between miR-493-5p and SNHG14 or myocyte enhancer factor 2 C (Mef2c) was confirmed by dual-luciferase reporter assay. Bone histomorphometry changes were evaluated to analyze SNHG14'roles in osteoporosis in vivo. Our results illustrated SNHG14 and Mef2c levels were increased in a time-dependent manner in BMSCs, and miR-493-5p expression was decreased. SNHG14 knockdown inhibited osteogenic differentiation of BMSCs, and SNHG14 upregulation had the opposite effect. SNHG14 overexpression elevated bone mineral density and bone trabecular number, and alleviated osteoporosis progression in vivo. Mechanically, miR-493-5p was a target of SNHG14, and miR-493-5p targeted the Mef2c gene directly. SNHG14 overexpression reversed the inhibition of miR-493-5p on the osteogenic ability of BMSCs, and miR-493-5p silencing accelerated BMSCs osteogenesis by activating Mef2c-mediated autophagy to accelerate BMSCs osteogenesis. In short, SNHG14 activated autophagy via regulating miR-493-5p/Mef2c axis to alleviate osteoporosis progression, which might provide a new molecular target for osteoporosis treatment.
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