Search Results (8,693)

Neurodegeneration with brain iron accumulation (NBIA) comprises a group of rare genetic movement disorders characterized by progressive neurological deterioration, dystonia, parkinsonism, spasticity, and abnormal iron deposition in the basal ganglia. Although iron accumulation is the shared neuroradiological hallmark, most NBIA genes do not directly regulate iron metabolism. Instead, major NBIA forms arise from disruption of distinct but converging cellular pathways, including coenzyme A (CoA) biosynthesis, lipid metabolism, mitochondrial function, and autophagy. This narrative review aims to examine the pathogenic mechanisms of major NBIA disorders, namely pantothenate kinase-associated neurodegeneration (PKAN), COASY protein-associated neurodegeneration (CoPAN), PLA2G6-associated neurodegeneration (PLAN), mitochondrial membrane protein-associated neurodegeneration (MPAN), and beta-propeller protein-associated neurodegeneration (BPAN), and how these insights are guiding therapeutic development. Preclinical strategies aimed at restoring CoA metabolism, improving mitochondrial function, limiting lipid peroxidation, modulating autophagy, or correcting the underlying genetic defect have shown encouraging results, although none have yet reached robust clinical validation. Clinical translation remains limited by disease rarity, clinical heterogeneity, absence of validated biomarkers, and preclinical models that only partially recapitulate human pathology. Advancing the field will depend on earlier molecular diagnosis, biomarkers capable of tracking disease stage, and trial designs suited to ultra-rare populations. NBIA thus offers a paradigm for how mechanistic classification of a genetically defined disease group can redirect therapeutic strategy away from a shared radiological feature and toward pathway-specific intervention. Full article

Background: Intraoperative hypotension (IOH) is the leading modifiable contributor to postoperative acute kidney injury (AKI), yet most evidence is associational and the heterogeneity of its effect is unknown. We estimated the causal effect of IOH burden on AKI and tested whether the most susceptible patients can be identified preoperatively. Methods: In a retrospective cohort of 2726 general-anesthesia cases from VitalDB, the exposure was the time-integrated mean arterial pressure (MAP) <65 mmHg burden (≥30, ≥60 and ≥120 mmHg·min) and the outcome was KDIGO-defined AKI within 7 days. The primary estimator was pre-treatment-adjusted augmented inverse-probability weighting (AIPW; doubly robust) with bootstrap 95% confidence intervals (CIs). Sensitivity analyses comprised a controlled-direct-effect model, negative control outcomes, E-values and vasopressor-stratified estimates. Effect heterogeneity was estimated with a causal forest; preoperative gradient-boosted models and decision-curve analysis assessed personalization and clinical utility. Results: AKI occurred in 205 (7.52%) cases. At 60 mmHg·min the AIPW risk difference was +3.00 percentage points (pp; 95% CI +0.84 to +5.26), with a monotonic dose–response (+2.78 to +7.62 pp across thresholds) and E-values rising from 2.08 to 3.44. The effect was concentrated in patients with elevated preoperative creatinine (conditional effect +9.86 pp, more than twice the cohort average). This susceptibility was recoverable from routine preoperative variables alone, with intraoperative waveform features conferring no measurable improvement (ΔAUROC −0.001). For predicting AKI itself, a parsimonious 4-feature preoperative score matched a 27-feature model (AUROC 0.775 vs. 0.768) and provided positive net benefit. Conclusions: Intraoperative hypotension burden shows a dose-dependent association with postoperative AKI that is consistent with a causal effect, concentrated in patients with reduced baseline renal reserve who are identifiable from routine preoperative data without intraoperative waveform infrastructure. Full article

Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease with limited treatment options. Here, we demonstrate that fucoxanthin (FUCO), a natural marine carotenoid, attenuates free fatty acid (FFA)-induced hepatocellular steatosis and inflammatory responses in vitro by targeting the EGR2-CD36 axis (EGR2, early growth response protein 2; CD36, cluster of differentiation 36). In FFA-induced hepatocyte models (HepG2, Hep3B, and AML12), FUCO significantly reduced lipid accumulation and inflammatory markers without cytotoxicity. Mechanistic studies revealed that FUCO specifically inhibited fatty acid uptake and transport by downregulating CD36, while triglyceride (TG) degradation remained unaffected. RNA sequencing identified EGR2 as a master regulator induced by FFA and suppressed by FUCO. Functional validation showed that EGR2 overexpression completely blocked FUCO’s lipid-lowering effects and restored CD36 expression, confirming that FUCO acts through EGR2-dependent CD36 inhibition. Bioinformatic analysis further supported EGR2-mediated regulation of CD36 via tumor necrosis factor (TNF) and sterol regulatory element-binding factor (SREBF) pathways. Collectively, our findings establish EGR2 as a critical molecular target for FUCO and provide mechanistic insights that may support its further evaluation in preclinical models for MASH therapy. Full article

Bone marrow aspirate concentrate (BMAC) is widely used as a source of mesenchymal stromal/stem cells (MSCs) for musculoskeletal regeneration; however, BMAC lacks essential bone marrow extracellular matrix (ECM) components, a critical component of the stem cell niche that regulates MSC survival, paracrine signaling, and regenerative capacity. We previously demonstrated that an ECM-retaining micronized bone marrow product (BMAX™) preserves pro-regenerative MSC phenotypes in vitro. Human bone marrow from a single donor was processed into conventional BMAC or BMAX™. Post-traumatic osteoarthritis was induced in immunodeficient rats using destabilization of the medial meniscus (DMM). Four weeks after surgery, animals were randomly assigned to receive intra-articular injections of BMAX™, BMAC, or phosphate-buffered saline (n = 10–12 in each group). Pain-related behavior (n = 5–6/group), histological assessment (n = 3–6/group), and micro-computed tomography (n = 4–6/group) were evaluated for up to 8 weeks after treatment. At 4 weeks after treatment, BMAC significantly increased the paw withdrawal threshold compared with PBS (p = 0.0068), whereas BMAX™ significantly reduced knee joint swelling compared with both PBS (p = 0.0235) and BMAC (p = 0.0039), and BMAX™ significantly improved knee bend scores compared with PBS (p = 0.0011). Neither treatment significantly improved OARSI histological scores at this time point. At 8 weeks after treatment, BMAX™ significantly increased the paw withdrawal threshold compared with PBS (p = 0.0305), whereas BMAC showed a non-significant trend (p = 0.0517); both treatments significantly reduced knee bend scores compared with PBS (p = 0.0027 and p = 0.0255), and BMAX™ demonstrated significantly lower knee bend scores than BMAC (p = 0.0090). BMAX™ significantly reduced knee swelling compared with PBS (p = 0.0196). Histologically, BMAX™ significantly improved OARSI scores in both the femoral condyle and tibial plateau compared with PBS (p = 0.0020 and p = 0.0003, respectively), whereas BMAC significantly improved only tibial plateau OARSI scores (p = 0.0014). Furthermore, BMAX™ demonstrated significantly lower femoral condyle OARSI scores than BMAC (p = 0.0243). Micro-computed tomography revealed that both BMAX™ and BMAC significantly reduced medial subchondral trabecular separation compared with PBS (p = 0.0340 and p = 0.0426, respectively), whereas no significant differences were observed between the two treatment groups for other bone structural parameters. In conclusion, preservation of the native bone marrow ECM was associated with improved functional outcomes and greater cartilage regeneration compared with conventional BMAC in this preclinical rat model of post-traumatic osteoarthritis. These findings support the concept that maintaining the native stem cell niche may enhance the therapeutic potential of bone marrow-derived cell therapies for osteoarthritis. Full article

The spread of multidrug-resistant (MDR) bacteria has renewed interest in combining the targeted killing of bacteriophages with immunomodulatory antimicrobial peptides (AMPs). AMPs offer broad antimicrobial, antibiofilm, and immunomodulatory effects, although their efficacy is limited by stability, delivery, and toxicity. Phage-based systems may help address some of these limitations by localizing antimicrobial activity and improving bacterial targeting. In this perspective, we treat engineered phages as programmable “Trojan horses” that deliver AMPs into their bacterial targets, framing this concept alongside the rapid growth of AI-guided AMP design as well as phage–host matching. The evidence thus far is largely preclinical. AMP-armed phages have shown activity in vitro and in animal models, while engineered phages have only recently entered early-phase clinical trials. Reasons why phage-delivered AMPs remain largely in the preclinical and early translational stages are delineated. We argue that the primary hurdle lies in the gap between the separate advancement of AMP design on one end and phage–host matching on the other. The alignment of these interests, along with manufacturing and regulatory efforts, will likely be what allows this therapy to reach the bedside. Full article

Huntington’s disease (HD) has traditionally been conceptualized as a neuron-centric disorder primarily attributed to cell-autonomous toxicity of mutant huntingtin (mHTT) in striatal medium spiny neurons. However, this framework inadequately explains the prolonged presymptomatic phase, selective network vulnerability, early non-motor manifestations, and limited success of neuron-targeted therapeutic interventions. Accumulating evidence from molecular biology, transcriptomics, neuroimaging, and preclinical therapeutics supports a reframing of HD as a disorder of neuroglial systems dysfunction. We synthesize data demonstrating that astrocytes, microglia, and oligodendrocyte lineage cells are not passive bystanders but play direct and interactive roles in HD pathogenesis through defined molecular mechanisms. Expression of mHTT in glial populations impairs synaptic homeostasis, metabolic coupling, immune resolution, and myelin integrity, generating self-amplifying pathological feedback loops that destabilize neural circuits long before overt neuronal death. Critically, we evaluate glial replacement therapy as a potential disease-modifying strategy. Preclinical studies demonstrate that transplantation of healthy human glial progenitor cells substantially ameliorates motor, cognitive, and neuropathological deficits in multiple HD models through oligodendroglial remyelination and lactate-mediated metabolic support, despite persistent neuronal mHTT expression. Effective HD therapy will likely require strategies that jointly target the genetic cause and the dysfunctional neuroglial microenvironment. By integrating systems neuroscience with glial biology and translational strategy, this review defines a neuroglial framework for HD that opens a plausible path toward meaningful disease modification and positions HD as a model disorder for glial-centric interventions in neurodegeneration. Full article

Hepatocellular carcinoma (HCC), a leading cause of cancer-related mortality worldwide, is driven by complex interactions between genetic mutations and reversible epigenetic alterations. Among these, aberrant DNA methylation, histone modifications, and dysregulated noncoding RNAs (ncRNAs) play central roles in hepatocarcinogenesis, tumor progression, and therapy resistance. Epigenetic changes not only regulate key oncogenic pathways, including JAK/STAT and RAS, but also contribute to tumor immune evasion and heterogeneity. Unlike genetic mutations, epigenetic alterations are reversible, offering unique opportunities for therapeutic targeting. This review highlights recent advances in understanding the epigenetic landscape of HCC, identifies promising biomarkers for early detection and prognosis, and evaluates emerging epigenetic therapies (including DNMT, HDAC, and BET inhibitors as well as ncRNA-based strategies). Although these therapies have shown tumor-suppressive or treatment-sensitizing effects in preclinical models, their clinical translation remains limited by modest efficacy, small early-phase trials, treatment-related adverse events, and insufficient biomarker-guided patient selection. These insights may support more precise diagnostic and therapeutic strategies for HCC. Full article

Background/Objectives: Diabetes mellitus type 2 (T2DM) is often associated with hypertension, necessitating treatment with combinations of medications that address both glycemic control and blood pressure. Whether commonly co-prescribed antihypertensives modify the glycemic efficacy of a sulfonylurea remains insufficiently characterized in controlled preclinical models. Methods: One hundred adult male Wistar rats were allocated to ten parallel groups (n = 10): healthy and diabetic untreated controls; glimepiride, bisoprolol or amlodipine monotherapy (in healthy and diabetic animals); and the diabetic combinations glimepiride+bisoprolol and glimepiride+amlodipine. T2DM was induced with a high-fat diet plus low-dose streptozotocin (35 mg/kg, i.p.) and confirmed by fasting blood glucose ≥ 200 mg/dL. Glycated hemoglobin (HbA1c) was measured weekly for 11 weeks. Non-parametric inference (Kruskal–Wallis, Dunn’s with Bonferroni correction, Mann–Whitney U, Wilcoxon signed-rank) was complemented by Random Forest regression and PCA/K-means clustering. Results: Week-11 HbA1c differed markedly across groups (Kruskal–Wallis H = 94.3, p < 0.001). Glimepiride + bisoprolol achieved near-normal control (4.37% ± 0.15), statistically indistinguishable from healthy groups (p ≥ 0.33), and was the only diabetic regimen with a declining trajectory (−0.66 percentage points; Wilcoxon p = 0.004). Adding either antihypertensive to glimepiride did not worsen glycemic control. Amlodipine monotherapy did not attenuate hyperglycemia (8.47% ± 0.20), approaching that of untreated diabetic controls (9.31% ± 0.18), consistent with the absence of intrinsic glucose-lowering activity. All agents showed pronounced disease-state dependence (healthy–diabetic divergence 2.33–3.13 points). Random Forest prediction was accurate (R² = 0.985), and unsupervised clustering separated effective from ineffective regimens, corroborating the statistical findings. Conclusions: In this model, bisoprolol co-administration enhanced and amlodipine co-administration preserved glimepiride-mediated glycemic control. Glimepiride+bisoprolol emerged as the most effective regimen, supporting cardioselective β-blockade as a metabolically favorable antihypertensive partner for sulfonylurea therapy and warranting clinical confirmation. More broadly, these results provide a preclinical, evidence-based rationale for selecting metabolically favorable antihypertensives in patients with coexisting T2DM and hypertension, with the potential to improve glycemic outcomes and reduce the risk of adverse drug–disease interactions during combination therapy. Full article

Background: C-reactive protein (CRP) is a well-established marker of systemic inflammation, while Growth Differentiation Factor-15 (GDF-15) has emerged as a potential biomarker of cellular stress. Their relative perioperative dynamics remain incompletely defined. This prospective observational study aimed to explicitly characterize and compare the longitudinal dynamics of CRP and GDF-15 in patients undergoing elective knee arthroplasty. Characterizing these biomarkers in a controlled acute surgical model provides clinical relevance by mapping systemic acute-phase inflammation against cellular stress pathways, which may offer a baseline reference for evaluating chronic tissue-wasting states. Methods: This prospective observational study included 47 patients undergoing elective knee arthroplasty. After excluding nine patients with elevated baseline CRP (>10 mg/L), serial measurements of CRP and GDF-15 were analysed daily in 38 patients from pre-operation to postoperative Days 1–3. Results: CRP rose sharply after surgery, peaking on Day 3 (median: 206.0 mg/L vs. baseline: 3.0 mg/L), representing a maximal increase exceeding 6100%. GDF-15 levels also increased progressively, peaking on Day 3 (median: 1682.5 pg/mL vs. baseline: 968.8 pg/mL), which represented a statistically significant but more modest rise of 33%. CRP and GDF-15 were significantly correlated on postoperative day 1 (rs = 0.53, p = 0.001) but not days 2 and 3. Baseline GDF-15, but not CRP, was significantly associated with oral hypoglycaemic agent use and vitamin B12 supplementation. Compared to values reported in recent randomized trials of ghrelin, anti-GDF-15, and anti-IL-6 therapies, GDF-15 levels in this surgical cohort remained lower, while CRP approached levels observed in such studies. Conclusions: CRP and GDF-15 rise in parallel following surgical injury; however, GDF-15 shows a considerably lower sensitivity to the inflammatory response. These findings suggest a complementary role of GDF-15 alongside CRP in profiling the perioperative stress response. While its relatively modest acute elevation limits its utility as a primary marker of acute inflammation, this surgical stress model serves as a reference that may help contextualize biomarker profiles in chronic inflammatory or wasting conditions, such as cancer cachexia, rather than serving as a direct tool for cachexia management. Full article

Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by oxidative stress, cholinergic dysfunction, and amyloid-β (Aβ) aggregation. Tri-Sannibat-Phol (TSB), a classical Thai polyherbal formulation comprising Piper retrofractum fruit, Ocimum tenuiflorum root, and Piper nigrum root, has been traditionally used for its medicinal properties, yet its anti-AD potential has never been scientifically evaluated. Methods: The therapeutic potential of TSB was investigated through in vitro bioassays including antioxidant, acetylcholinesterase (AChE) inhibitory, and anti-Aβ aggregation assays, alongside neuroprotective evaluation in H₂O₂-induced SH-SY5Y neuroblastoma cells. Acute oral toxicity was assessed in male ICR mice in accordance with OECD Guideline 420. Cognitive-enhancing effects were evaluated using the modified Y-maze, Novel Object Recognition, and Morris Water Maze tests in a scopolamine-induced amnesic mouse model. LC-MS/MS analysis was performed for phytochemical characterization and chemical standardization of the formulation. Results: TSB demonstrated significant antioxidant activity, AChE inhibitory activity, and anti-Aβ aggregation effects, with P. nigrum and O. tenuiflorum identified as the primary contributing components. Neuroprotective effects were confirmed in H₂O₂-induced SH-SY5Y cells, where TSB significantly improved cell viability across concentrations of 1–100 µg/mL. Acute oral toxicity assessment revealed an LD₅₀ exceeding 2000 mg/kg, indicating a favorable safety profile. In vivo behavioral studies demonstrated that TSB at medium-to-high doses significantly reversed scopolamine-induced cognitive deficits across all three behavioral tests. LC-MS/MS analysis identified thirteen piperidine alkaloids, with piperine as the dominant constituent at 17.61 ± 0.80% w/w, proposed as the primary bioactive driver and chemical marker for future quality standardization. Conclusions: These findings suggest that TSB exerts multi-targeted anti-AD effects through complementary mechanisms, supporting its potential as a traditional medicine-based therapeutic candidate for further preclinical and clinical investigation. Full article

Purpose: Most children with autism live in resource-limited settings with limited access to timely interventions. To address this gap, the World Health Organization developed Caregiver Skills Training (CST) to support caregivers and expand intervention access globally. This study examined the feasibility and preliminary outcomes of a modified CST in mainland China. Methods: Using the ecological validity model and qualitative interviews, the CST materials were culturally adapted and modified for the Chinese context. A pre- and post-test controlled trial was conducted with caregivers of children with autism aged 2–9 years, who were assigned to either the CST intervention group (N = 15) or a caregiver education control group (N = 15). Clinical outcomes for caregivers and children were evaluated at baseline and after a 10-week intervention period. Results: Cultural adaptation and modifications focused on language adjustments, localization of case examples and demonstrations, and optimization of teaching methods and training schedules. Supplementary within-group analyses indicated pre–post changes in caregiver knowledge and skills, parenting stress, and selected child outcomes, including speech/language/communication, sensory/cognitive awareness, and overall autism symptoms. However, most between-group differences were not statistically significant after baseline adjustment. Conclusions: The findings provide preliminary evidence for the feasibility of culturally adapted and modified CST in mainland China. Given the pilot nature of the study and the absence of statistically significant between-group effects for most outcomes, the outcome findings should be interpreted as exploratory and hypothesis-generating rather than evidence of efficacy. Further large-scale studies with greater statistical power and objective outcome measures are needed to evaluate effectiveness and implementation feasibility. Full article

Background:Ulva lactuca (sea lettuce) is a green macroalgae rich in sulfated polysaccharides (ulvans), polyphenols, and pigments with documented antioxidant and anti-inflammatory activity in preclinical models. Translational human data remain limited. Methods: Twenty healthy adults (20–35 years; BMI 18.5–30 kg/m²) were enrolled in a single-center, randomized, double-blind, placebo-controlled, parallel-group trial (CTRI/2025/11/097278) and assigned 1:1 to receive 300 mg of an U. lactuca extract or matched placebo once daily for 28 days. Antioxidant biomarkers (GSH, MDA, catalase, GPx-1, thioredoxin) and inflammatory biomarkers (CRP, IL-6, IL-1β, IL-11, PPAR-γ) were measured at Day 0 and Day 28. Safety was assessed throughout. Results: Eighteen of 20 participants completed the study. Compared with placebo, U. lactuca produced significant within-group improvements at Day 28 in GSH (+4.04 ng/mL), GPx-1 (+67.8 µU/mL), and catalase (+32.4 kU/L) and reductions in MDA (−6.08 nmol/mL) and thioredoxin (−1.48 ng/mL); inflammatory markers CRP (−0.91 mg/L), IL-6 (−2.97 pg/mL), IL-11 (−4.28 ± 1.88 ng/mL) and IL-1β (−8.87 pg/mL) decreased and PPAR-γ increased. Conclusions: In this short-duration pilot trial, daily supplementation with 300 mg of an U. lactuca extract was well tolerated and modulated systemic oxidative-stress and low-grade inflammatory biomarkers in healthy adults. Larger and longer studies in populations with elevated oxidative stress are warranted. Full article

Background: Metastatic liver tumors (MLT) and parasitic liver cysts (PLC) are common liver conditions that often exhibit similar imaging characteristics, making accurate diagnosis challenging using imaging alone. This overlap can result in diagnostic errors and delayed treatment, particularly in resource-limited settings or when invasive procedures such as biopsies are not feasible due to risk or unavailability. This study aimed to develop a reliable and transparent machine learning approach to distinguish MLT from PLC using radiomic features derived from computed tomography (CT). Methods: We propose an explainable radiomics-based machine learning framework for the non-invasive, accurate, and interpretable discrimination of MLT and PLC, designed to assist radiologists in reducing diagnostic ambiguity and expediting patient management. This retrospective study included 30 adult patients, comprising 15 with liver metastases and 15 with pathologic hepatic cysts. Radiomic features were extracted from pre-treatment CT scans using PyRadiomics. Feature selection was performed using three complementary methods: Mutual Information, Lasso regression, and LightGBM importance ranking. HistGradientBoosting classifiers were then trained on each selected feature set. Results: Model performance was evaluated using 5-fold cross-validation and assessed with ROC AUC, accuracy, precision, recall, and F1-score. SHAP analysis was applied to interpret the models and identify key radiomic biomarkers. Statistical comparisons were performed using DeLong’s test for AUCs, McNemar’s test for classification agreement, and paired t-tests for metrics such as accuracy and F1-score. The Mutual Information-based model achieved the highest mean AUC (0.9717 ± 0.0267), significantly outperforming the other models (p < 0.035). Key features contributing to classification included texture entropy, interquartile range, and gray level non-uniformity. Conclusion: We developed a robust and interpretable machine learning framework for differentiating metastatic liver tumors from parasitic liver cysts using CT-derived radiomic features. The integration of Mutual Information feature selection, ensemble learning, and SHAP explainability ensured high diagnostic accuracy, strong calibration, and transparency. The proposed framework demonstrates substantial clinical relevance and holds promise for real-world implementation. Full article

Objective: Survival prediction in oncology and cardiology requires models that can capture nonlinear prognostic structure while remaining interpretable, calibrated, and clinically safe. This study develops and evaluates a diagnostic-first hybrid quantum–classical framework for right-censored survival analysis. Methods: We introduce KTA-Survival (Kernel-Target Alignment for survival), a pre-training feasibility diagnostic that adapts kernel-target alignment to censored outcomes by comparing a quantum fidelity kernel with a concordance-based survival target kernel. We then propose QResid-Boost (Quantum Residual Boosting), a Cox-LASSO–anchored residual framework in which a variational quantum circuit is trained on martingale residuals through a Quantum-Skip-Residual architecture. A sigmoid-bounded scalar gate, α, constrains the quantum contribution and allows the model to reduce to the classical baseline when the residual signal is uninformative. The framework was evaluated on GBSG2 (German Breast Cancer Study Group 2; n = 686), FLChain (serum free light chain; n = 1500), WHAS500 (Worcester Heart Attack Study; n = 500), and a synthetic Weibull positive-control dataset containing high-frequency periodic interactions. Results: On the GBSG2 hold-out partition, Random Survival Forest achieved the highest concordance (C = 0.7188), followed by the Stacking ensemble (C = 0.7128), Cox-LASSO (C = 0.7019), and QResid-Boost (C = 0.7016). The leading classical and hybrid models did not differ significantly by paired bootstrap testing, whereas all outperformed the pure quantum variants. In the synthetic positive-control cohort, QResid-Boost improved over Cox-LASSO by ΔC = +0.0397, demonstrating that the quantum residual can add value when nonlinear periodic structure remains after the linear baseline. KTA-Survival yielded positive ΔKTA values across the evaluated datasets and correctly identified the regime in which the quantum residual produced its largest measurable gain. Conclusions: The proposed diagnostic-first framework reframes quantum survival modelling as a gated enrichment strategy rather than an unconstrained replacement for classical risk models. In low-dimensional clinical cohorts where linear structure already explains most prognostic signal, the framework behaves conservatively; when residual nonlinear structure is present, it can provide measurable improvement without uncontrolled model drift. Full article

Eucalyptus globulus is a widely cultivated medicinal species of recognized phytochemical richness and broad preclinical relevance across multiple biological and formulation-oriented application domains. This review aimed to integrate the available evidence on the botanical identity, phytochemical profile, preclinical biomedical relevance, and translational considerations within a single structured framework. A bibliometric-assisted narrative review approach was applied, based on targeted literature retrieval from scientific platforms (e.g., PubMed, ScienceDirect, MDPI, Google Scholar), complemented by keyword co-occurrence analysis and qualitative narrative synthesis. The reviewed literature indicates that E. globulus is characterized by a 1,8-cineole-rich essential oil together with non-volatile phenolic, flavonoid, and related secondary metabolites that support a wide range of reported biological activities. The strongest preclinical evidence concerns antimicrobial and antibiofilm effects in oral-health-related models, antioxidant and anti-inflammatory activity, respiratory relevance, wound-healing support, selected cytotoxicity-related effects, and emerging nano-enabled delivery systems. Overall, E. globulus represents a promising multifunctional species with substantial preclinical potential; however, direct clinical evidence remains limited, and future progress will depend on better phytochemical standardization, mechanistic clarification, and well-designed translational studies. Full article