Search Results (10,179)

Background/Objectives: Morin is the first flavonoid isolated from plants in the Moraceae family and has been reported to exhibit anticancer and antioxidant activity. It is classified as a Class IV compound in the Biopharmaceutical Classification System due to its low water solubility and low permeability. This study aimed to develop and characterize morin-loaded liposomes composed of DPPC and cholesterol to improve their stability and anticancer activity. Methods: Liposomes were prepared by thin-film hydration and then processed by bath sonication, probe sonication, or membrane extrusion to control vesicle size. Formulations were characterized by hydrodynamic diameter, polydispersity index (PDI), zeta potential, encapsulation efficiency (EE), and colloidal stability over 7 days at 37 °C. The cytotoxic effects of free and encapsulated morin were evaluated in tumor (MDA-MB-231, B16F10) and non-tumor (NIH-3T3, HEK-293T) cell lines. Results: Extrusion yielded the most homogeneous liposomes (PDI = 0.2, size ≈ 90 nm), whereas sonication methods produced larger, more polydisperse vesicles. EE ranged from 11–17%, with no significant differences among methods. Free morin degraded by 40% at 37 °C after 7 days, whereas liposomal encapsulation significantly reduced degradation, preserving 82–89% of the compound. At a morin equivalent of 3.4 µM, the bath-sonicated formulation reduced viability to approximately 65% in MDA-MB-231 cells and 70% in B16F10 cells, whereas viability remained approximately 86% in NIH-3T3 cells and 82% in HEK-293T cells. All formulations maintained colloidal stability over the study period. In cytotoxicity assays, free morin showed minimal activity, whereas liposomal formulations significantly enhanced antiproliferative effects against cancer cells. Conclusions: These findings demonstrate that DPPC/cholesterol liposomes effectively stabilize morin and improve its bioactivity, representing a promising strategy for delivering this flavonoid in anticancer therapies. Full article

Maternal chronic conditions, including obesity, diabetes, hypertensive disorders, and autoimmune diseases, promote a systemic proinflammatory environment characterized by oxidative stress and chronic inflammation. These alterations lead to reduced expressions of human leukocyte antigen-G (HLA-G) and programmed death-ligand 1 (PD-L1), decreased regulatory T (Treg)cell activity, and increased T helper (Th)1/Th17 responses, disrupting placental immune privilege and resulting in increased production of proinflammatory cytokines, oxidative stress, trophoblastic dysfunction, and placental senescence. This change in immune privilege contributes to fetal growth restriction, preterm birth, congenital anomalies, and long-term cardiometabolic programming in offspring. Understanding the mechanisms underlying placental immune dysregulation may facilitate the development of targeted therapeutic strategies aimed at restoring immune tolerance and reducing inflammatory and hypoxic signaling pathways to improve maternal and neonatal outcomes. This review summarizes the current state of the field of placental immunological privilege and how maternal chronic conditions like obesity, diabetes, hypertensive disorders, and autoimmune diseases can disrupt it and its possible consequences on the progeny. Full article

Background/Objectives: Glioblastoma multiforme (GBM) remains the most aggressive and treatment-refractory primary brain tumor, with current therapeutic modalities providing minimal survival improvement. Chimeric antigen receptor (CAR)-based immunotherapies succeeded in hematologic malignancies but are constrained in solid tumors by tumor heterogeneity, immunosuppressive microenvironment, and delivery challenges. CD276 (B7-H3), a pan-cancer antigen overexpressed in gliomas and correlated with poor patient outcomes, represents a compelling immunotherapeutic target. Methods: Here, we developed a non-viral lipid nanoparticle (LNP)-based platform for transient CAR mRNA delivery to T cells and evaluated its application for generating CD276 (B7-H3)-targeted CAR-T cells against GBM. An in-house-assembled T-mixer incorporating polyether ether ketone (PEEK) tubing was integrated with a dual-syringe-pump system for controlled LNP production. Results: LNPs formulated with clinically relevant ionizable lipids, SM-102 and DLin-MC3-DMA, demonstrated high encapsulation efficiency and effective mRNA delivery. Cell-type-dependent expression kinetics were further characterized following LNP-mediated reporter mRNA delivery in K562, NK, NK92, and T cells, revealing differences in transgene expression across cell populations. LNP-mediated delivery of CD276 CAR mRNA enabled generation of CAR-expressing T cells that exhibited antigen-specific cytotoxicity against CD276-positive LN229 GBM cells in vitro. Conclusions: Collectively, this study demonstrates the feasibility of an adaptable LNP-based platform for non-viral CAR mRNA engineering of T cells and CD276-targeted cytotoxicity against GBM cells in vitro. The combination of transient CAR expression and LNP-mediated mRNA delivery provides a foundation for further optimization and evaluation in preclinical in vivo models. Full article

Ulcerative colitis (UC) is a chronic inflammatory disease in which epithelial barrier injury, microbial perturbation, dysregulated mucosal immunity, and altered neural signaling converge. Although dysbiosis is frequently reported in UC, taxonomic shifts alone do not explain how microbial signals are translated into mucosal inflammation, urgency, pain, relapse, or heterogeneous therapeutic responses. This review develops a focused framework of gut microbiota -driven neuroimmune crosstalk, defined as bidirectional communication through which microbial communities and their metabolites regulate epithelial, neuronal, glial, enteroendocrine, and immune compartments, while neural and immune signals reshape barrier function and microbial ecology. We synthesize evidence on short-chain fatty acids, tryptophan-derived indoles, serotonin signaling, bile acids, microbe-associated molecular patterns, vagal anti-inflammatory reflexes, enteric neurons, sensory neurons, enteric glia, macrophages, dendritic cells, T cells, innate lymphoid cells, mast cells, and neutrophils. Therapeutic opportunities include diet, prebiotics, probiotics, postbiotics, fecal microbiota transplantation, metabolite-based interventions, vagus nerve stimulation, neuropeptide or serotonin pathway modulation, and combination strategies with established anti-inflammatory therapies. UC-specific evidence is emphasized where available, with explicit distinction between human UC findings, broader inflammatory bowel disease (IBD) evidence, experimental colitis models, and general mechanistic studies. A microbiota–neuroimmune framework may help move UC research beyond descriptive dysbiosis toward mechanism-guided precision therapy; however, most causal neuroimmune pathways still require validation in well-phenotyped human UC cohorts, and the proposed endotypes in this review are hypothesis-generating and require prospective validation. Full article

A series of 11 compounds of phenyl–imidazole–pyrrole and 9 compounds of phenanthryl–imidazole–pyrrole were synthesized and evaluated against breast cancer cell lines differing in the expression of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor (HER)-2, viz., BT-474 (ER+, PR+, and HER2+), T-47D and MCF-7 (ER+, PR+, and HER2−), and MDA-MB-468 and MDA-MB-231 (ER−, PR−, and HER2−). The analysis of the results indicated that the most active compounds were 5d and 5k from the phenyl–imidazole–pyrrole series and 6b and 6i from the phenanthryl–imidazole–pyrrole series (IC₅₀ < 50 µM). Molecular docking (MD) and molecular dynamics simulation (MDS) studies demonstrated that the active compounds exhibited high binding affinity to the 7NH5 (a co-crystal structure of Akt1 and its specific inhibitor) protein, which is overexpressed in many breast cancer types. The active compounds 6b and 6i reduced the viability of MDA-MB-231 and MCF-7 cells by inducing cell death mechanisms. Both compounds halted the proliferation by arresting cells in the G0/G1 phase of the cell cycle. The results are similar to those of traditional Cisplatin. Intraperitoneal administration of 6i retarded the development of EAC tumors and increased the survival of mice compared with tumor-bearing control and 5-fluorouracil (5FU)-treated positive control mice. Full article

Macrophages play an important role in bone regeneration by releasing bioactive factors that regulate the behavior of osteoprogenitor cells. In this in vitro study, we investigated how conditioned media (CM) derived from RAW 264.7 macrophages treated with lipopolysaccharide (LPS; 1 or 100 ng/mL), dexamethasone (DEX; 10⁻⁶ M), or left untreated, modulate the proliferation and osteogenic differentiation of MC3T3-E1 preosteoblasts. Exposure to LPS and DEX produced different patterns of macrophage activation, assessed by microscopic morphology, nitroblue tetrazolium (NBT) reduction, and measurement of TNF-α secretion from macrophages. In the L929 bioassay, no CM was cytotoxic, while effects on MC3T3-E1 proliferation and differentiation varied with macrophage treatment and CM dilution. CM obtained from DEX-treated macrophages elicited the most pronounced pattern of osteogenic activity that included reduced cell proliferation, acquisition of osteoblast-like morphology, enhanced von Kossa staining, and pronounced osteocalcin and osteopontin immunoexpression. CM from untreated macrophages also supported osteogenesis, although to a lesser extent. At 100%, CMs from LPS-treated macrophages supported greater preosteoblast proliferation than other CMs, while their effects on differentiation depended on LPS dose and CM dilution. These findings indicate that macrophage-derived signals differentially modulate preosteoblast proliferation and differentiation depending on their functional state. This study provides a valuable in vitro cell model for the development of immunomodulatory and regenerative strategies in bone tissue engineering and broader applications in wound healing. Full article

The rapid growth of urban populations and consumption patterns has significantly increased the volume and complexity of municipal waste streams, including recyclable, organic, hazardous, and electronic waste. Traditional waste management approaches such as manual sorting and fixed collection schedules struggle to handle the diversity and scale of modern waste systems efficiently. Consequently, recent research has explored artificial intelligence (AI), computer vision, and Internet of Things (IoT) technologies to automate waste classification and enable intelligent monitoring and management of waste infrastructures. However, the rapidly expanding literature in this domain is fragmented across different datasets, sensing platforms, and experimental settings, making it difficult to obtain a comprehensive understanding of current technological progress. To address this gap, this study conducts a systematic literature review using the PRISMA methodology, analyzing 50 rigorously selected peer-reviewed studies on automated waste classification and intelligent waste management systems. The protocol was registered in the Open Science Framework (OSF). The reviewed works are examined in terms of model architectures, sensing infrastructures, datasets, and system capabilities. The analysis shows that convolutional neural network architectures such as ResNet, MobileNet, and EfficientNet, together with object detection frameworks including YOLO and Faster R-CNN, dominate current visual waste classification research; however, emerging studies increasingly explore hybrid architectures combining convolutional networks with transformer-based models to improve contextual understanding and scalability. IoT-enabled smart bins equipped with ultrasonic sensors, load cells, and environmental sensors are widely used for real-time waste monitoring. The review also reveals a recent surge of research activity, particularly in Asia, with increasing contributions from major publishers such as Elsevier and MDPI. Despite promising experimental performance, most systems remain limited to small curated datasets and pilot-scale deployments, highlighting a gap between laboratory research and real-world implementation. These findings provide a consolidated overview of current research trends and identify key challenges for developing scalable and practical intelligent waste management systems. Full article

The autoimmune regulator (AIRE) is essential for central immune tolerance, but its role in thymic epithelial cell (TEC) differentiation and development remains incompletely understood. To address this, we knocked down AIRE in mouse embryonic stem cells (mESCs) and analyzed thymic epithelial progenitor (TEP) differentiation using RNA-sequencing and also performed thymic AIRE knockdown in NOD/Ltj mice to evaluate type 1 diabetes (T1D) pathogenesis. AIRE knockdown significantly reduced the proportion of K5⁺/K8⁺ TEPs among EpCAM1⁺ cells and altered the ECM–receptor interaction pathway, with downregulation of SPP1 and upregulation of Fn1 and CD44. Importantly, re-expression of AIRE using an shRNA-resistant rescue vector partially reversed these molecular changes and partially restored TEP differentiation. In vivo, thymic AIRE knockdown accelerated blood glucose elevation, aggravated insulitis, and reduced expression of T1D-associated TSAs (INS2, GAD67) and maturation markers (CD80, MHC-II). Importantly, the changes in SPP1, Fn1, and CD44 were consistent between in vitro and in vivo models. Furthermore, AIRE deficiency increased CD4⁺ single-positive thymocytes, reduced splenic Treg frequency, and enhanced antigen-specific T cell proliferation and activation. Collectively, these findings demonstrate that AIRE deficiency impairs TEP differentiation and alters the ECM-receptor pathway, while thymic AIRE deficiency compromises immune tolerance and accelerates T1D progression in NOD/Ltj mice. Full article

Background/Objectives: Hematopoietic stem cell transplantation (HSCT) is a life-saving treatment for many hematological disorders, but demand for unrelated donors continues to outpace donor-registry growth. Voluntary blood donors are a strategic population for donor recruitment, yet their HSCT knowledge and attitudes remain understudied. This study examined these and their relationship with sociodemographic characteristics, blood donation behaviors, and each other. Methods: This cross-sectional, descriptive study was conducted with 300 voluntary blood donors aged 18–64 years attending a blood transfusion and apheresis center in Istanbul, Türkiye, between June and October 2025. Face-to-face interviews used a researcher-developed, content-validated Donor Information Form (scale-level content validity index = 0.96; Kuder–Richardson-20 = 0.828 for knowledge and 0.863 for attitude). Data were analyzed using descriptive statistics, t-tests, ANOVA, Pearson correlation, and linear regression. Results: Mean knowledge and attitude scores were low (31.85 ± 21.82 and 34.98 ± 26.63 out of 100, respectively). Healthcare professional status, prior HSCT awareness, and previous stem cell donation were each associated with significantly higher knowledge and attitude scores (all p < 0.001), with the largest effect observed for previous donation experience on attitude (d = 1.92). Knowledge and attitude were strongly correlated (r = 0.705, p < 0.001), and knowledge predicted attitude (R² = 0.496, p < 0.001). Although 29.3% of participants had considered stem cell donation, only 1.7% had ever donated—a gap that also reflects the need to be matched with a recipient. Conclusions: Knowledge and attitudes regarding HSCT among voluntary blood donors were generally insufficient, with a marked gap between donation intention and actual behavior. Knowledge strongly predicted attitude. Nurse-led education at blood donation encounters, combined with simplified donor-registry enrollment, may help expand the pool of registered stem cell donors. Full article

Dedifferentiated liposarcoma (DDLPS) of the spermatic cord is an exceptionally rare and aggressive malignancy for which diagnostic and therapeutic guidelines remain limited. We report the case of a 73-year-old man who presented with a rapidly enlarging left inguinal/paratesticular mass. Initial ultrasonography showed a 4.3 × 3.0 × 3.7 cm hypoechoic lesion interpreted as suggestive of leiomyoma. Pelvic magnetic resonance imaging subsequently demonstrated a 10 × 5 × 5 cm neoplastic mass arising from the spermatic cord. The patient underwent radical left orchiectomy. Histopathological examination revealed a high-grade spindle-cell neoplasm with marked pleomorphism and up to 30 mitoses per 10 high-power fields. Immunohistochemistry showed positivity for p16, MDM2, and CDK4, with a Ki-67 proliferative index of 95%, supporting the diagnosis of high-grade DDLPS. Although surgical margins were negative, the disease progressed rapidly. Nineteen days after surgery, the patient developed bilateral pleural effusion, pleural infiltration, pulmonary metastases, and a probable pathological T11 fracture. Because of extensive metastatic disease and clinical deterioration, systemic antineoplastic therapy was not initiated in this advanced setting. The patient died 27 days after hospitalization due to progressive metastatic disease. This case highlights the diagnostic difficulty, aggressive biological behavior, and need for early multidisciplinary management of spermatic cord DDLPS. Full article

The receptor for advanced glycation end products (RAGE/AGER) is an important mediator of inflammatory signaling and has been implicated in chronic low-grade inflammation associated with aging. Chronic low-grade inflammation (“inflammaging”) is a characteristic feature of biological aging, providing a rationale for investigating molecular regulators of inflammatory signaling such as RAGE. This study aimed to develop and validate short hairpin RNA (shRNA) constructs suppressing AGER/RAGE in human cell models. Five shRNA constructs targeting human AGER were designed, cloned into pLSL-puro, and verified by Sanger sequencing. Lentiviral vectors were produced in HEK293T cells and used to establish stable HEK293T, 786-O, and human umbilical vein endothelial cell (HUVEC) populations with AGER knockdown. AGER/RAGE expression was assessed by RT-qPCR, Western blotting, and flow cytometry. Silencing efficiency varied with the construct and the cellular model. sh1 produced the strongest suppression of AGER, exceeding 70% in selected models, whereas sh2 was effective in HEK293T and 786-O cells. Reduced RAGE expression was confirmed at the mRNA, protein, and cell-surface levels, identifying sh1 and sh2 as lead candidates. An AGER-focused workflow for lentiviral shRNA construct screening and experimental validation was established, providing a reproducible approach for generating stable cell models with reduced AGER/RAGE expression. Further work is required to confirm isoform specificity, assess off-target effects, and define the functional consequences of RAGE suppression. Full article

Type 2 diabetes mellitus (T2DM) and osteoarthritis (OA) are highly prevalent chronic disorders with increasing global burdens that frequently coexist and share common risk factors, including obesity, aging and chronic low-grade inflammation. This narrative review aims to summarize current evidence regarding the epidemiological, clinical and molecular links between T2DM and OA and to highlight potential therapeutic implications. Growing evidence suggests that T2DM contributes to OA development and progression through multiple interconnected mechanisms. These include advanced glycation end-product (AGE) accumulation, oxidative stress, chronic inflammation, extracellular matrix degradation, impaired autophagy, ferroptosis, mesenchymal stem cell dysfunction and microvascular impairment within joint tissues. In addition, shared genetic and molecular pathways, including AGE–RAGE, IL-17, PI3K/Akt/mTOR and LGR6/Wnt/β-catenin/NRF2 signaling, further support a biological connection between the two diseases. Clinically, T2DM is associated with increased OA severity, enhanced pain sensitization, accelerated disease progression and higher rates of joint arthroplasty. Emerging evidence also suggests that antidiabetic agents, particularly metformin and glucagon-like peptide 1 receptor agonists, may exert disease-modifying effects through anti-inflammatory, metabolic and chondroprotective mechanisms. Overall, T2DM and OA should be regarded as interconnected metabolic-inflammatory disorders. Improved understanding of their shared mechanisms may facilitate earlier intervention, therapeutic repurposing and integrated multidisciplinary management strategies to reduce disease burden and improve patient outcomes. Full article

Enterotoxigenic Escherichia coli (ETEC) is a major pathogen responsible for diarrhea and mortality in piglets, causing substantial economic losses to the swine industry. Its pathogenicity relies on the synergistic action of colonization factors and enterotoxins, which mediate intestinal colonization and induce secretory diarrhea. Commercial vaccines against ETEC remain limited, and their protective efficacy in piglets is often unsatisfactory. Consequently, probiotics have attracted increasing attention as mucosal immunomodulatory agents for the prevention and control of ETEC infection. In this study, ETEC, the minor subunit located at the tip of the fimbriae, FaeC, and the fimbrial assembly accessory protein, LngC, were individually inserted into Lactiplantibacillus plantarum NC8 using the anchoring expression vector pPG612.1, successfully generating the recombinant strains NC8/pPG612.1-FaeC and NC8/pPG612.1-LngC. Western blot analysis confirmed that both recombinant strains correctly expressed the target proteins upon lactose induction, and their growth curves exhibited no significant differences from those of the wild-type strain, indicating that genetic modification did not compromise bacterial proliferation. To evaluate the immune efficacy of the recombinant strains, thirty-six piglets were randomly assigned to six groups: PBS control, ETEC challenge, empty vector, LngC immunization, FaeC immunization, and combined immunization (MIX). After seven oral gavage immunizations, piglets were challenged with ETEC and euthanized on day 7 post-challenge for sample collection. The results showed that immunized piglets resumed body weight gain by day 4 after challenge, whereas the ETEC group exhibited sustained weight loss. Histopathological examination revealed relatively intact jejunal villus architecture and markedly less severe mucosal damage in immunized groups compared with the ETEC-challenged group. RT-qPCR analysis of intestinal tissues and ELISA analysis of serum showed that immunization with the recombinant strains significantly decreased the mRNA expression of pro-inflammatory cytokines (TNF-α, IL-6, and IL-8) in intestinal tissues and their protein levels in serum, while increasing both the mRNA expression and protein levels of the anti-inflammatory cytokine IL-10. Flow cytometric analysis revealed that immunization with the recombinant strains significantly increased the frequencies of CD4⁺IFN-γ⁺ and CD4⁺IL-4⁺T cells and CD21⁺ B cells in MLNs, LPLs, and spleen compared with the control groups. The increased CD4⁺IFN-γ⁺ T-cell population indicated enhanced Th1-mediated cellular immunity, whereas the increased CD4⁺IL-4⁺ T-cell population suggested activation of Th2-associated humoral immunity. The expansion of CD21⁺B cells further indicated enhanced B-cell activation. Collectively, these findings suggest that the recombinant strains induced coordinated mucosal and systemic immune responses. Additionally, the secretory immunoglobulin A (sIgA) concentration in the jejunal contents was markedly increased, suggesting that the intestinal mucosal immune system was effectively activated. Collectively, these findings indicate that NC8/pPG612.1-FaeC and NC8/pPG612.1-LngC can elicit robust mucosal immune responses and alleviate diarrhea induced by enterotoxigenic Escherichia coli (ETEC) in piglets, providing a scientific basis for the development of oral probiotic-based vaccines against ETEC infection in swine. Full article

Hyperlipidemia is a widespread metabolic disease that triggers abnormal lipid accumulation. Plant polyphenols possess great potential for lipid metabolism regulation. Small-leaved kuding tea (Ligustrum robustum Roxb. Blume, SLKDT) is abundant in polyphenols with proven hypolipidemic activity, whereas its key active constituents and molecular targets remain unclear. This study aimed to identify the key active components and core targets responsible for the lipid-lowering effects of SLKDT polyphenols. Response surface methodology (RSM) was employed to optimize the extraction process of SLKDT polyphenols. In vitro cell experiments were performed to verify the lipid-lowering effect of SLKDT polyphenols, while the obtained polyphenols were further qualitatively characterized via LC-MS/MS. Furthermore, network pharmacology prediction combined with molecular docking was used to screen the key bioactive compounds and their target proteins associated with lipid metabolism regulation. Under the optimal extraction conditions (43% ethanol concentration, ultrasound time of 40 min, solid-to-liquid ratio of 1:56 g/mL, and ultrasonic temperature of 57 °C), the yield of polyphenols from SLKDT was 131.88 mg/g. In vitro experiments confirmed that SLKDT polyphenols significantly reduced intracellular lipid accumulation in HepG2 cells, increased the activities of antioxidant enzymes including GSH-PX, CAT, and T-SOD, and decreased MDA content. Furthermore, SLKDT polyphenols markedly downregulated the expression of lipid synthesis-related genes, including ACC, HMGCR, SREBP-1c, and FASN, while upregulating CYP7A1 expression. A total of 88 compounds were Preliminary identified by LC-MS/MS, mainly including glycosides, flavonoids and phenolic acids. Network pharmacology analysis revealed that chrysin, 6-demethoxytangeretin, bavachinin, isobavachin, and bavachalcone were the core components mediating the lipid-lowering activity of SLKDT polyphenols, with target proteins including TP53, STAT3, AKT1, HSP90AA1, and EGFR. This study elucidates the key components and critical targets underlying the lipid-lowering effects of SLKDT polyphenols, providing experimental evidence and theoretical support for the development of SLKDT-derived products and natural lipid-lowering agents. Full article

Critical-sized bone defects remain a major clinical challenge because of their limited regenerative capacity and the high incidence of delayed healing and non-union. Biomorphic calcium phosphate scaffolds have emerged as promising bone tissue engineering (BTE) platforms owing to their ability to reproduce the hierarchical architecture of trabecular bone while providing a bioactive environment for bone regeneration. In the present study, the early osteogenic transcriptional response of biomorphic magnesium-doped hydroxyapatite (HA)/β-tricalcium phosphate (β-TCP) scaffolds obtained through biomorphic transformation of a rattan wood template was investigated to evaluate their ability to support the early osteogenic response of pre-osteoblastic cells. Porous scaffolds preserving the hierarchical architecture of the rattan template and exhibiting different HA/β-TCP phase compositions were obtained through a multistep biomorphic transformation process followed by controlled magnesium incorporation. Cytocompatibility was assessed using MC3T3-E1 pre-osteoblastic cells by evaluating cell viability, adhesion and proliferation. The early osteogenic response was investigated by analyzing the expression of representative osteogenic marker genes in cells cultured on the scaffolds under basal and osteogenic conditions. All scaffold formulations were cytocompatible and supported cell adhesion and proliferation. Culture on biomorphic Mg²⁺-doped HA/β-TCP scaffolds promoted the expression of osteogenic marker genes, and this response was further enhanced following osteogenic stimulation. No statistically significant differences among the investigated formulations were detected in cell viability or osteogenic marker gene expression. Overall, these findings demonstrate that biomorphic Mg²⁺-doped HA/β-TCP scaffolds provide a favorable microenvironment for pre-osteoblastic cell growth and early osteogenic transcriptional commitment. The present work also establishes a simplified experimental model for investigating the contribution of magnesium to the early osteogenic transcriptional response of biomorphic calcium phosphate scaffolds, providing a rational basis for the development of next-generation bone graft substitutes. Full article