ArticleMolecular biology reports2024
COL6A3 enhances the osteogenic differentiation potential of BMSCs by promoting mitophagy in the osteoporotic microenvironment.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- From mechanisms to therapeutics: a narrative review on pyroptosis and autophagy in osteoporosis.Annals of medicine · 2025Pooled it
- Oxygen-vacancy-engineered t-ZnO-CeOBioactive materials · 2026Article
- A Modular Bioinstructive Platform Reveals Mechanistic Insights into Additive-Free, Topography-Driven Osteogenesis.Advanced healthcare materials · 2026Article
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- Article
- 17β-estradiol promotes osteogenic differentiation of BMSCs by regulating mitophagy through ARC.Journal of orthopaedic surgery and research · 2025Article
- Autophagy: regulating the seesaw of bone-fat balance.Frontiers in cell and developmental biology · 2025Review
- Mitochondrial Transplantation: A Paradigm Shift in Osteoporosis Therapy.International journal of nanomedicine · 2025Review
- Deciphering oligomeric proanthocyanidins' dual osteoprotective mechanisms at single-cell resolution:Frontiers in immunology · 2025Article
- Novel perspectives on autophagy-oxidative stress-inflammation axis in the orchestration of adipogenesis.Frontiers in endocrinology · 2024Review
- Identification of potential pathogenic genes related to osteoporosis and osteoarthritis.Technology and health care : official journal of the European Society for Engineering and Medicine · 2024Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBone marrow mesenchymal stem cells (BMSCs) have been widely recognized as a highly promising option for cell-based tissue engineering therapy targeting osteoporosis. However, the osteogenic differentiation of BMSCs is impeded by the limited viability and diminished capacity for bone formation within the osteoporotic microenvironment.
methodsIn this study, the COL6A3 gene was confirmed through an extensive analysis of the preceding single-cell sequencing database. The generation of an inflammatory microenvironment resembling osteoporotic cell transplantation was achieved by employing lipopolysaccharide (LPS). A lentivirus targeting the COL6A3 gene was constructed, and a Western blotting assay was used to measure the marker proteins of osteogenesis, adipogenesis, and mitophagy. Immunofluorescence was utilized to observe the colocalization of mitochondria and lysosomes. The apoptosis rate of each group was evaluated using the TUNEL assay, and the mitochondrial membrane potential was assessed using JC-1 staining.
resultsThis investigation discovered that the impaired differentiation capacity and decreased viability of BMSCs within the inflammatory microenvironment were markedly ameliorated upon overexpression of the specific COL6A3 gene. Moreover, the administration of COL6A3 gene overexpression successfully mitigated the inhibitory impacts of LPS on mitophagy and the expression of inflammatory mediators, specifically inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in BMSCs. To clarify the underlying mechanism, the role of mitophagy during the differentiation of COL6A3 gene-modified BMSCs in the inflammatory microenvironment was evaluated using the mitophagy inhibitor Mdivi-1.
conclusionsIn the context of lipopolysaccharide (LPS) stimulation, COL6A3 enhances the differentiation of BMSCs into osteogenic and adipogenic lineages through the promotion of mitophagy and the maintenance of mitochondrial health. Our findings may provide a novel therapeutic approach utilizing stem cells in the treatment of osteoporosis.
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