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Reconstruction of critical-size bone defects remains a persistent clinical challenge after trauma, tumour resection and degenerative disease. Nanoparticles (NPs) have emerged as versatile platforms that couple tunable material properties with targeted molecular delivery to direct regeneration. This review synthesizes advances from the past decade across inorganic (for example, nanostructured hydroxyapatite and bioactive glasses), polymeric, lipid, and bioinspired NPs, and links key design parameters—size, shape, mechanics, surface chemistry and degradability—to osteogenic outcomes. We examine how NPs steer stem-cell fate through mechanotransduction and canonical signaling (Wnt/β-catenin, BMP/Smad, MAPK), and highlight emerging mechanisms including controlled ion release, redox modulation, protein-corona dynamics and macrophage immune reprogramming toward pro-healing phenotypes. Three key modes of translational application are emphasized: NPs as carriers for proteins, nucleic acids and small molecules; as bioactive or reinforcing components within load-bearing scaffolds; and as injectable microenvironments that provide spatiotemporal control of cell signaling cues. Ongoing clinical applications in dental, orthopedic and spinal therapeutics show growing adoption, while also revealing gaps in long-term safety, Good Manufacturing Practices (GMP), and regulation. In future developments, stimuli-responsive and self-reporting nanomaterials, informed by AI-guided design and integrated with 3D bioprinting, offer routes to patient-specific grafts with predictable performance. By consolidating mechanisms into practical design rules, we chart a path from tunable nanoscale interfaces to reliable, clinically impactful bone regeneration. 

Free fatty acid (FFA) production in bacteria is a key target for metabolic engineering. The knockout of the acyl-ACP synthetase (AAS) prevents reincorporation of FFA into the fatty acid biosynthetic cycle and is widely used to enhance their secretion. However, the role of AAS in membrane lipid remodeling under environmental stress, such as altered temperature, remains poorly understood. In cyanobacteria, temperature shifts are known to affect fatty acid desaturation and membrane fluidity, yet it is unclear whether AAS contributes to these adaptive responses through re-esterification of membrane-released acyl chains. We elucidated unique aspects of fatty acid metabolism in response to temperature changes in biotechnologically relevant microbes with the development of an efficient method for quantifying acyl-ACP intermediates using anion exchange chromatography (AEX). In Escherichia coli, which performs desaturation during fatty acid biosynthesis, we detected saturated and unsaturated acyl-ACPs that confirm biosynthetic pathway operation. In the cyanobacteria, Picosynechococcus sp. PCC 7002 and the Δaas strain, changes between two temperatures were interpreted with support from proteomic and lipidomic analyses and indicated that the AAS is tied to membrane lipid remodeling. Further, polyunsaturated acyl-ACPs were detected in the Δaas strain, which was unexpected because fatty acid synthesis does not produce polyunsaturates in cyanobacteria, suggesting the presence of alternative acyl-activating enzymes or unknown acyl-ACP desaturases. This study highlights the possible link between acyl chain recycling and lipid remodeling in cyanobacteria and demonstrates the utility of AEX-based acyl-ACP profiling in dissecting fatty acid metabolism. 

Adipocyte differentiation plays an important role in bone remodeling due to secretory factors that can directly modulate osteoblast and osteoclast, thus affecting overall bone mass and skeletal integrity. Excessive adipocyte differentiation within the bone marrow microenvironment can lead to decreased bone mass, eventually causing osteoporosis. The mechanical microenvironment of bone marrow, including fluid shear, maintains the balance of adipocyte and osteoblast differentiation during bone remodeling. However, how mechanical cues interact with long noncoding RNA (lncRNA) and regulate adipocyte differentiation remains unexplored. In this study, we investigated the mechanosensitive role of lncRNA MALAT1 during mesenchymal stem cells (MSCs) adipocyte differentiation. By applying physiologically relevant shear stress, MSCs experienced morphological changes and adipocyte differentiation differences. Shear stress inhibits adipocyte differentiation of MSCs, demonstrated by reduced oil-red-o-stained lipid droplets. Silencing MALAT1 also results in reduced adipocyte differentiation. By leveraging a novel gapmer double stranded locked nuclei acid nanobiosensor, we showed that shear stress inhibits MALAT1 expression, with significantly reduced fluorescence intensity. Our findings indicate that shear stress influences adipocyte differentiation mainly through the downregulation of MALAT1, highlighting a significant interplay between biophysical cues and lncRNAs. This interaction is crucial for understanding the complexities of bone remodeling and the potential therapeutic targeting of lncRNAs to treat bone-related disorders. 

NMR metabolomics was applied toM. mercenariaexposed to a series of sublethal doses of Brevetoxins for the targeted metabolic pathway and early marker discovery. 

Bone-derived nanoparticles enhance osteogenic differentiation of mesenchymal stem cells through upregulating Dll4 expression.