ArticleStem cell research & therapy2025
The role of PKM2-mediated metabolic reprogramming in the osteogenic differentiation of BMSCs under diabetic periodontitis conditions.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Mitochondrial hub: the integrative axis connecting ferroptosis and metabolic reprogramming in periodontitis.Molecular biology reports · 2026Review
- Circadian disruption and cellular senescence: emerging perspectives in periodontitis.Odontology · 2026Review
- Drynaria roosii-derived exosome-like nanovesicles promote alveolar socket healing via activation of ITPR3-mediated calcium flux.Journal of nanobiotechnology · 2026Article
- Acarbose modulates microglial Pkm2 acetylation to reshape immunometabolism and preserve retinal neurons after ischemia-reperfusion.Journal of neuroinflammation · 2026Article
- Bioengineered extracellular vesicles escape lysosomal degradation and deliver Tet-PKM2 for macrophage immunometabolic reprogramming and periodontitis treatment.Bioactive materials · 2026Article
- miR-500a-3p negatively regulates SOCS2 and participates in the proliferation, glycolysis, and apoptosis of HCC cells via the JAK2/STAT5 pathway.Journal of applied biomedicine · 2026Article
- Asiatic Acid-Loaded Hydrogel Ameliorates Diabetic Periodontitis via Mitophagy-Mediated M2 Macrophage Polarization.ACS omega · 2026Article
- Obesity and bone health: reconciling the density-fragility paradox.Frontiers in endocrinology · 2026Review
- Delactylase effects of SIRT3 on a positive feedback loop involving the RUNX1-glycolysis-histone lactylation in diabetic kidney disease.International journal of biological sciences · 2026Article
- The regulatory effects of PD-1/PD-L1 inhibitors on bone metabolism: opportunities and challenges in osteoporosis management.Frontiers in immunology · 2025Review
- Mechanisms and therapeutic perspectives of mitochondrial dysfunction of macrophages in periodontitis.Frontiers in cellular and infection microbiology · 2025Review
- From "immune silence" to "immune dialogue": modification strategies for bone substitutes based on bone immunomodulatory characteristics.Frontiers in cell and developmental biology · 2025Review
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6 authors.
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Abstract
backgroundDiabetes mellitus (DM) and periodontitis have a bidirectional relationship, with each being a high-risk factor for the other. Prolonged hyperglycemia exacerbates periodontal inflammation and disrupts bone homeostasis. Pyruvate kinase M2 (PKM2), a key enzyme in glycolysis, is involved in metabolic reprogramming, but its role in osteogenesis under high-glucose (HG) inflammatory conditions remains largely unknown. This study aimed to investigate the effects of HG and inflammation on bone marrow mesenchymal stem cells (BMSCs) under indirect co-culture conditions and to explore how PKM2 regulates metabolism and mitochondrial function during osteogenic differentiation in HG inflammatory environments, elucidating its role in diabetic periodontitis (DP).
methodsExpose BMSCs to conditioned medium (CM) collected from RAW264.7 cells stimulated with HG and/or lipopolysaccharide (LPS). BMSCs functionality was assessed using CCK8, EdU, Annexin V-PI apoptosis assay, alkaline phosphatase (ALP), and Alizarin Red S (ARS) staining. Metabolic characteristics were evaluated through Seahorse assays, lactate production, glucose uptake, and ATP measurements. Mitochondrial function was assessed via JC-1, and ROS staining, Mito-Tracker staining, and transmission electron microscopy (TEM). Gene and protein expression were analyzed by quantitative real-time PCR and western blotting. In vivo therapeutic effects of shikonin were validated via micro-CT and histological staining in a diabetic periodontitis mouse model.
resultsIn vitro experiments demonstrated that HG inflammatory conditions impaired the survival of BMSCs, suppressed osteogenic differentiation, and induced metabolic reprogramming. This reprogramming was characterized by enhanced glycolysis, impaired oxidative phosphorylation (OXPHOS), abnormal upregulation of PKM2 expression, and mitochondrial dysfunction accompanied by morphological alterations. Shikonin effectively reversed these adverse effects by inhibiting PKM2 tetramerization, rescuing the loss of osteogenic function in BMSCs. The therapeutic potential of shikonin was confirmed in the diabetic periodontitis mouse model.
conclusionPKM2 impairs the osteogenesis of BMSCs by affecting metabolism and mitochondrial function, suggesting it as a potential therapeutic target for diabetic periodontitis.
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