ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Targeted Delivery of α-ketoglutarate to Macrophages in Bone: A Novel Therapeutic Strategy for Improving Fracture Healing in Type 2 Diabetes.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Ternary mTOR-targeted conductive nanofibrous scaffolds with bioactive peptides orchestrate immune-metabolic-fibrotic balance for diabetic bone regeneration.Bioactive materials · 2026Article
- From metabolic node to smart building block: α-Ketoglutarate-empowered biomaterials for programmable cell fate.Materials today. Bio · 2026Review
- Reprogramming macrophage immunometabolism via glutamine antagonism potentiates colorectal cancer therapy in mice.Nature communications · 2026Article
- Liposomal multimodal theranostics for bone disorders: from rational responsive delivery and biomimetic strategies to clinical translation.Journal of nanobiotechnology · 2026Review
- Smart immunomodulatory polysaccharide hydrogels promote diabetic bone regeneration by regulating the inflammation-angiogenesis-osteogenesis axis.Materials today. Bio · 2026Article
- Immunometabolism of macrophages in the bone microenvironment: a new perspective for bone healing therapy.Journal of advanced research · 2026Review
- Metabolic reprogramming in diabetic complications: mechanisms, pathologies, and molecular evidence from multi-organ studies.Frontiers in immunology · 2026Review
- Targeted Delivery of α-ketoglutarate to Macrophages in Bone: A Novel Therapeutic Strategy for Improving Fracture Healing in Type 2 Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Impaired fracture healing is a common complication in type 2 diabetes mellitus (T2DM), with limited effective treatments. This study investigates the role of macrophages in bone repair and introduces a novel therapeutic strategy. Reduced glutaminase (GLS) expression and glutaminolysis are found in macrophages from T2DM mice and monocytes from T2DM patients. Specific deletion of GLS in macrophages altered their phenotypes and delayed fracture healing in mice. Mechanistically, GLS deficiency reduced α-ketoglutarate (α-KG) levels in macrophages, which impairs bone morphogenetic protein 2 (BMP2) production by increasing cytosine methylation on the promoter, ultimately hindering osteogenic differentiation of bone marrow mesenchymal stem cells. Importantly, while systemic α-KG supplementation deteriorates fracture healing in T2DM mice, a targeted delivery of α-KG using α-KG@Cy5.5@ALN-Liposome to macrophages in bone markedly improves fracture healing. These findings underscore the critical role of macrophage glutaminolysis in fracture healing and propose targeted α-KG delivery as a promising therapeutic intervention for improving fracture repair in T2DM patients.
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Registered trials
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.