Search Results (1,518)

Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a major cause of morbidity and mortality worldwide, particularly due to the emergence of drug-resistant strains. Membrane-active antimicrobial peptides (AMPs) represent attractive therapeutic candidates because they target bacterial envelope integrity and disrupt essential cellular processes. We evaluated two rationally designed LL-37-derived peptides: a truncated C-terminally amidated analog (LL37-1) and a modified variant incorporating N-terminal acetylation and a single D-amino acid substitution (D-LL37). Dose–response analysis demonstrated that D-LL37 exhibited greater antimycobacterial potency, with lower inhibitory concentrations of 90% (IC₉₀) and 50% (IC₅₀) values (18.40 ± 0.39 μM and 10.11 ± 0.60 μM, respectively) compared with LL37-1 (25.44 ± 0.36 μM and 15.45 ± 1.40 μM). Fluorescence-based permeability assays revealed partial membrane disruption (36% and 44% at IC₉₀ for LL37-1 and D-LL37, respectively), which was supported by ultrastructural alterations observed by scanning electron microscopy, including bacillary shortening, rough surface formation, cell clusters, and the presence of cellular debris, all of which are consistent with membrane damage. RT-qPCR analysis demonstrated significant upregulation of the P-type ATPase genes ctpF, ctpA, and ctpH following D-LL37 exposure. Collectively, these findings indicate that optimized LL-37-derived peptides exert antitubercular activity associated with envelope perturbation and coordinated activation of ion transport-related stress responses. Full article

The olfactory and gustatory systems are essential for survival, enabling organisms to detect and respond to environmental chemical cues. Although canonical signaling pathways in smell and taste have been well defined, growing evidence highlights additional ion channel families as key modulators of sensory responses. Recent studies identify the anoctamin, transmembrane channel-like, and TMEM63 superfamily as a class of non-canonical sensory effectors that regulate signal amplification, excitability, and epithelial homeostasis across chemosensory systems. In the mammalian olfactory epithelium, specific anoctamin channels enhance odor-evoked responses and contribute to tissue homeostasis. In the gustatory system, salt detection is now understood to involve multiple parallel signaling pathways, with TMC4 emerging as a key contributor to high-salt and salt-associated taste sensing. These channel families are evolutionarily conserved across species, including C. elegans, Drosophila, and aquatic organisms, where they mediate chemosensation, mechanosensation, humidity detection, and osmoregulation. This functional versatility is supported by a shared structural architecture that enables selective ion conduction and, in some members, regulated phospholipid scrambling. This review proposes a unifying framework in which anoctamin and transmembrane channel-like proteins act as multimodal regulators of sensory signaling, linking environmental cues to cellular excitability and microenvironmental control and highlighting new principles of chemosensory organization and therapeutic potential. Full article

Background/Objectives: Alzheimer’s disease (AD) remains a progressive neurodegenerative disorder with limited therapeutic options. This study aimed to develop an integrative multi-omics computational pipeline to identify diagnostic biomarkers and prioritize druggable therapeutic targets for AD. Methods: We integrated transcriptomic data from 1047 samples (547 AD, 500 controls) using weighted gene co-expression network analysis (WGCNA) and three machine learning algorithms (LASSO, Random Forest, SVM) with strict separation of training, feature selection, and evaluation. Single-cell RNA sequencing of 48,481 nuclei from entorhinal cortex, two-sample Mendelian randomization (MR) with Bayesian colocalization, and structure-based molecular docking with triplicate 500 ns molecular dynamics (MD) simulations were also employed. Results: Machine learning identified 10 consensus biomarker genes involved in synaptic vesicle cycling, ion transport, and calcium homeostasis (internal test AUC = 0.891, 95% CI: 0.836–0.946; external validation on GSE48350: AUC = 0.847, 95% CI: 0.798–0.896). Covariate-adjusted differential expression and MR with Bayesian colocalization converged on eight immune-related therapeutic targets including APOE, TREM2, and TYROBP ($p<0.05$; Bonferroni-corrected threshold $p<0.00625$). Single-cell analysis revealed oligodendrocyte expansion in AD (28.5% versus 24.8%), with target genes predominantly expressed in microglia and astrocytes. Virtual screening of 2634 FDA-approved drugs prioritized 10 exploratory repurposing candidates; indomethacin–TREM2 and celecoxib–CSF1R are primary exploratory candidates given structurally validated binding pockets. Triplicate MD simulations (15 $\mathsf{\mu }$s aggregate) showed force-field-consistent structural stability (RMSD ≤ 3.2 Å). A quantitative multi-omics convergence framework identified four Tier 1 targets (APOE, TREM2, TYROBP, CX3CR1) supported by ≥5 analytical layers ($P_{\mathrm{perm}}=0.0003$; note: three of five layers share the same transcriptomic input). Conclusions: These findings provide a multi-evidence computational framework linking diagnostic biomarkers and druggable neuroinflammatory targets for AD. All predictions require experimental validation in biochemical and cellular models before clinical conclusions can be drawn. Full article

Objectives: This study characterised the bioactive properties (i.e., ion release, pH rise, and apatite formation) of a newly developed Voco Profluorid + BioMin F varnish. Three additional varnishes were investigated for comparison: Clinpro™ White Varnish (3M™, St. Paul, MN, USA), MI Varnish (GC, Tokyo, Japan), and Profluorid varnish (VOCO GmbH, Cuxhaven, Germany). The Clinpro™ White and MI varnishes were chosen for comparison due to their similar composition of active ingredients. Profluorid served as a standard fluoride-only varnish reference. Methods: Dental varnish ingredients were characterised using ATR-FTIR, XRD, and ¹⁹F and ³¹P MAS-NMR. Coated coverslips were immersed in Tris buffer and artificial saliva (pH 4.0 and 7.0) for 2–24 h. Ion release was analysed using ICP-OES and a fluoride ion-selective electrode whilst monitoring pH changes. Post-immersion, coverslips were analysed by XRD and MAS-NMR to assess possible apatite formation. Results: XRD and ¹⁹F MAS-NMR detected NaF in all four varnishes. BioMin F varnish showed a ³¹P peak matching BioMin F glass, with an additional brushite peak, indicating partial reaction of the bioactive glass (BAG) with rosin resin water. All varnishes released fluoride and calcium, but only BioMin F and MI varnishes released phosphate, which is essential for the formation of calcium fluorapatite. Post-immersion analysis confirmed fluorapatite formation in BioMin F and, to a lesser extent, the Profluorid varnish. No apatite formation was observed in the other two varnishes. MI varnish exhibited calcium fluoride formation before and after immersion, as evidenced by XRD and ¹⁹F MAS-NMR analysis. Conclusions: The novel BioMin F varnish potentially promotes remineralisation by providing a sustained and slow release of therapeutic ions that are essential for the formation of fluorapatite. Full article

Nosema ceranae is a common and highly contagious fungal pathogen that primarily infects the gut of adult honeybees, causing nosemosis. As a chronic disease of the digestive system, it poses a global threat to honeybee health and colony sustainability. This study aimed to investigate the inhibitory effects of different concentrations of Scutellaria baicalensis aqueous extract on N. ceranae in the intestines of infected Apis cerana through feeding experiments. In addition, the therapeutic efficacy of its major active component, baicalin, was evaluated, and its potential molecular mechanisms of action were explored. The results showed that, compared with the control group, administration of S. baicalensis aqueous extract at concentrations of 1 mg/mL, 5 mg/mL, and 10 mg/mL significantly reduced midgut spore loads (p < 0.05). Further experiments showed that a 0.5 mg/mL baicalin sucrose solution, prepared with 0.5% (v/v) DMSO as co-solvent, exhibited optimal solubility and significantly inhibited the proliferation of spores in the honeybee midgut. Transcriptomic analysis of A. cerana revealed varying numbers of significantly differentially expressed genes among the baicalin-treated (HG) group, the co-solvent control (DMSO) group, and the blank control (C) group. Four candidate DEGs associated with the effects of baicalin were further identified, namely LOC108003965, LOC108000905, LOC107996681, and CYP4G11. Gene Ontology enrichment analysis showed that, in the comparison between the HG group and the C group, these DEGs were significantly enriched in six functional categories: iron ion binding, phosphoric ester hydrolase activity, heme binding, tetrapyrrole binding, hydrolase activity (acting on ester bonds), and oxidoreductase activity (acting on paired donors, with incorporation or reduction of molecular oxygen). Collectively, these results demonstrate that S. baicalensis aqueous extract effectively inhibits the proliferation of N. ceranae within the host, and its active component, baicalin, exhibits a similar inhibitory effect. The present study proposes a novel strategy in which baicalin may enhance host endogenous chitinase-related activity to target and disrupt the spore wall, offering a new perspective for the prevention and control of honeybee nosemosis. Full article

Alzheimer’s disease (AD) develops as a progressive dementia condition through the step-by-step breakdown of nerve cells. Neurodegeneration in this context primarily results from metal ions, including copper, iron, zinc, and aluminum, building up in the system. The aggregation of amyloid-beta (Aβ) peptides and oxidative stress generation stem from metal ion involvement acting as defining characteristics of Alzheimer’s disease pathology. We developed a comprehensive mathematical model based on 24 coupled ordinary differential equations (ODEs) to represent the interactions between metal ions, Aβ peptides, reactive oxygen species (ROS), antioxidant defenses, and tau protein phosphorylation. The mathematical model monitors how metal ion concentrations change over time and examines their competitive binding effects, which trigger a series of reactions, resulting in oxidative stress and subsequent tau protein damage. The model uses analytical and numerical mathematical methods to expose nonlinear behaviors and threshold effects while offering mechanistic insights into the course of disease development. This model functions as a quantitative framework for assessing how therapeutic interventions that target metal dyshomeostasis and oxidative stress can potentially affect outcomes. Full article

This review provides a comprehensive overview of the modulatory actions of plant-derived constituents on membrane ion channels in various cell types. Among their diverse bioactivities, ion channel regulation—governing membrane excitability, signal transduction, and cellular homeostasis—has emerged as a critical mechanistic basis for their pharmacological effects. Twenty-four representative phytoconstituents are discussed and classified into five major categories based on their structural features: alkaloids, terpenoids, lignans and acetogenins, polyphenols, and other aromatic and conjugated compounds. Across these categories, the reviewed compounds exhibit distinct and often highly specific effects on the amplitude and gating kinetics of multiple ionic currents, including voltage-gated Na⁺ currents (I_Na), delayed-rectifier K⁺ currents (I_K(DR)), M-type K⁺ currents (I_K(M)), hyperpolarization-activated cation currents (I_h), erg-mediated K⁺ currents (I_K(erg)), inwardly rectifying K⁺ currents, and Ca²⁺-activated K⁺ currents (I_K(Ca)). Alkaloids predominantly suppress voltage-gated K⁺ currents, with notable exceptions such as aconitine, which alters the properties of both I_Na and I_K(DR), thereby contributing to its proarrhythmic toxicity. Terpenoids, including cannabidiol, croton diterpenoids, lutein, thymol, and triptolide, exert multifaceted effects on I_K(M), I_h, inwardly rectifying K⁺ currents, and Ca²⁺-activated K⁺ channels. Lignans and acetogenins, such as gomisin A, honokiol, sesamin, and squamocin, primarily modulate I_Na, I_h, and I_K(Ca), with several compounds demonstrating strong links between ion-channel modulation and anti-neoplastic or neuroprotective actions. Polyphenolic compounds, including curcumin, eugenol, resveratrol, gastrodigenin, gastrodin, and pterostilbene, display diverse ion-channel targeting profiles, influencing multiple Na⁺ and K⁺ channel subtypes. Other aromatic or conjugated compounds, such as isoplumbagin, plumbagin, and verteporfin, regulate I_K(erg) and I_K(Ca), potentially contributing to both therapeutic efficacy and adverse effects. Collectively, the compound-specific modulation of current amplitude and gating kinetics offers valuable mechanistic insight into the pharmacological and toxicological significance of plant-derived natural products, highlighting the functional role of ion channel evaluation in guiding their therapeutic development and ensuring safety assessment. Full article

Bortezomib (BTZ), the first-generation proteasome inhibitor, has been approved for the treatment of relapsed, refractory, and newly diagnosed multiple myeloma. Despite its remarkable antitumor efficacy, BTZ treatment is severely limited by a high incidence of systemic adverse reactions, primarily due to its non-selective cytotoxicity toward rapidly dividing normal cells and its potent neurotoxic effects on peripheral neurons. Bortezomib-induced peripheral neurotoxicity (BIPN) manifests as neuropathic pain and sensory abnormalities, affecting up to 31% to 64% of patients and limiting BTZ’s clinical use. Currently, the underlying mechanisms of BIPN are poorly understood. To evaluate the effects of BTZ on the functions of peripheral nerves in mice, we administered an intraperitoneal injection treatment for four weeks. Results indicated that BIPN caused mechanical allodynia, gait abnormalities, and pathological changes in myelin and axons in mice. This study confirms that BTZ upregulates the expression of the activating transcription factor 3 (ATF3), which in turn mediates the increased expression of the copper transporter SLC31A1, causing dysregulation of intracellular copper ion homeostasis and subsequent copper accumulation, and ultimately inducing the development of peripheral neurotoxicity. Elevated intracellular copper concentration exerts a dual effect: it directly promotes the oligomerization of Dihydrolipoamide S-acetyltransferase (DLAT) and concurrently damages the iron–sulfur cluster protein ferredoxin 1 (FDX1), collectively triggering the onset of cuproptosis. Green tea has garnered attention for its rich content of catechins, with (−)-Epigallocatechin Gallate (EGCG) being the most abundant catechin present. This study uncovers the molecular mechanism by which EGCG inhibits BTZ-induced cuproptosis through targeted regulation of copper homeostasis. Analyses demonstrate that EGCG significantly downregulates the expression of the copper transporter SLC31A1, thereby effectively suppressing transmembrane influx of extracellular copper ions. This intervention markedly reduces intracellular copper overload, eliciting a dual regulatory effect: on one hand, the decreased copper concentration directly inhibits the oligomerization of DLAT; on the other hand, it effectively protects the iron–sulfur cluster protein FDX1 from damage. This study aims to systematically elucidate the molecular mechanisms underlying BIPN and to evaluate the therapeutic potential of EGCG in alleviating BIPN, offering a novel therapeutic strategy for the prevention and treatment of BIPN. Full article

Bartter syndrome (BS) represents a group of rare, autosomal recessive renal tubular disorders characterized by hypokalemic hypochloremic metabolic alkalosis, secondary hyperaldosteronism, and normal to low blood pressure. The underlying pathophysiology is primarily driven by defects in critical ion transport proteins or channels localized within the thick ascending limb of the loop of Henle, leading to impaired salt reabsorption. Recent advances in molecular genetics have refined the classification of Bartter syndrome. Current evidence supports SLC12A1, KCNJ1, CLCNKB, BSND, and MAGED2 as the core disease genes within the contemporary BS spectrum, with MAGED2 causing a distinct X-linked transient antenatal form. In contrast, gain-of-function CASR variants, historically labeled “type V Bartter syndrome”, are now more appropriately described as CaSR-associated Bartter-like phenotypes within the broader spectrum of disorders of calcium homeostasis. Despite significant progress, two primary research limitations remain. First, fully elucidating genotype–phenotype correlations and overcoming diagnostic complexities continues to be highly challenging due to substantial phenotypic overlap and genetic heterogeneity. Compounding these diagnostic hurdles is the equally critical challenge of understanding mutation-driven pathogenic mechanisms to develop viable clinical interventions. This review systematically summarizes the current molecular genetic landscape of BS to address these gaps. We highlight the relationships between specific genetic variants and clinical manifestations, delve into molecular pathophysiology including protein misfolding and trafficking defects, and explore emerging therapeutic approaches such as molecular chaperones. By integrating genetic and clinical data, this work aims to provide a comprehensive framework to facilitate precise diagnosis and individualized treatment strategies, ultimately advancing precision medicine in the management of Bartter syndrome. Full article

Background/Objectives: Patient-derived mesenchymal stem cells (MSCs) represent a promising avenue for myocardial regeneration, yet therapeutic application remains limited by inconsistent differentiation capacity and the absence of standardized cardiogenic induction protocols. This study demonstrates a proof-of-concept for guiding patient-specific bone marrow MSCs toward a functional cardiomyocyte phenotype using paracrine signals from differentiating iPSC-derived cardiomyocytes (iPSC-CMs). Materials and Methods: MSCs were maintained in conditioned medium from a concurrent, validated iPSC-CM differentiation protocol, with evaluation via immunocytochemistry, optical mapping, and whole-cell patch-clamp recordings. Results: Differentiated MSCs acquired organized sarcomeric architecture with cross-striations and displayed spontaneous calcium oscillations with decay kinetics matching source iPSC-CMs (CaT50 ≈ 283 ms vs. 301 ms). In co-culture, MSC-derived cells exhibited synchronized calcium dynamics with iPSC-CMs, confirming functional coupling, while patch-clamp detected hallmark cardiac ion currents (INa, ICa,L, and IKv). Morphologically, MSC-CMs displayed more mature, elongated rod-like shapes. Conclusions: Although current densities indicate partial immaturity, their reproducible detection validates successful cardiomyogenic commitment. This “parallel differentiation” platform eliminates donor-specific protocol tuning, providing a streamlined, paracrine-mediated approach to generate autologous cardiomyocyte-like cells for disease modeling, pharmacological testing, and future regenerative applications. Full article

DNA damage requires repair via the endonuclease IV-mediated base excision repair (BER) pathway, which corrects apurinic/apyrimidinic (AP) sites. Chlamydophila pneumoniae AP endonuclease IV (CpEndoIV), the sole AP endonuclease in this pathogen, is crucial for genomic integrity. As humans lack a homologous protein, it represents a potential therapeutic target. In this study, we report the first crystal structure of CpEndoIV at 1.97 Å resolution. The structure reveals two Zn²⁺, one Mg²⁺, and a malonate molecule bound in the active site, marking the first observation of Mg²⁺ coordination in the EndoIV family. Compared to the three-Zn²⁺ model with a narrow, deep pocket for precise AP-site cleavage, the Zn²⁺/Mg²⁺-bound state has a wider, shallower pocket that might promote diverse catalytic activities. Combined with enzymatic assays, we suggest that the mixed Zn²⁺/Mg²⁺ model is better adapted for CpEndoIV to operate under host oxidative stress. Malonate binds to the metal ions, occupying the positions normally coordinated by water molecules. This binding mode may mimic the coordination of the substrate to the metal ions, and the protein conformation resembles that of the enzyme upon substrate binding at the active site. This study provides a structural basis for the functional characterization of CpEndoIV and offers a reference for the development of targeted inhibitors against diseases caused by Chlamydophila pneumoniae. Full article

Background/Objectives: Chronic metabolic acidosis (CMA) is a mild, persistent acid–base imbalance characterized by low serum bicarbonate and urinary pH and is common in chronic illness, aging, and metabolic disorders such as type 2 diabetes (T2D). This review highlights the critical, yet often overlooked, role of CMA in T2D (CMAD) and its contribution to disease pathophysiology. Methods: We conducted a comprehensive review of the systemic impacts of CMA, from molecular mechanisms to organ-specific dysfunction. The analysis covers physiological pH dynamics in intracellular (IC) and extracellular (EC) fluids and explores their effects on cellular processes, including the cell cycle and apoptosis. Results: At the molecular level, acidosis significantly alters enzyme kinetics, macromolecule metabolism, and ion conductance. Cell-level analysis shows that pH shifts impact proliferation and programmed cell death. Systemically, the manifestations of CMA align closely with T2D features in vital organs, including the pancreas, liver, skeletal muscle, adipose tissue, and the renal, nervous, and immune systems. Our findings indicate that the pathophysiological landscape of T2D largely mirrors the biological effects of chronic acidosis. Conclusions: The alignment between the effects of CMA and the clinical features of T2D suggests that T2D pathophysiology is worth revisiting through the lens of CMAD. This perspective is further supported by therapeutic interventions showing preliminary efficacy signals in limited studies of acid-neutralization in managing T2D symptoms and progression. Full article

Secondary caries and biofilm accumulation remain major causes of failure in provisional crowns and restorations, highlighting the need for multifunctional resin coatings with antibacterial and remineralizing capabilities. This study aimed to develop a novel bioactive and antibacterial resin-based surface coating incorporating 10% dimethylaminododecyl methacrylate (DMADDM), 20% nanoparticles of amorphous calcium phosphate (NACP), and/or 20% calcium fluoride nanoparticles (nCaF₂) within a urethane dimethacrylate/triethylene glycol divinylbenzyl ether (UDMA/TEG-DVBE) matrix. Coatings were evaluated for degree of conversion (DC), flow, shear bond strength, brushing wear resistance (10,000 cycles), and calcium (Ca), phosphate (PO₄), and fluoride (F) ion release up to 70 days. All groups achieved clinically acceptable polymerization, with the lowest DC at 50%. NACP-containing coatings significantly increased shear bond strength to 18.3 ± 2.8 MPa, representing a ~170% increase compared with the experimental control (6.8 ± 2.1 MPa) and exceeding the ISO 10477 minimum threshold of 5 MPa. After brushing simulation, experimental coatings demonstrated low wear depth (0.93–1.19 µm), which was ~40% lower than the commercial control (1.85 ± 0.40 µm). Sustained ion release was achieved for 70 days, with 20% NACP-formula releasing 1.22 mmol/L Ca and 0.90 mmol/L PO₄, while the dual NACP–nCaF₂ formulation provided simultaneous Ca (0.62 mmol/L) and F (0.33 mmol/L) release. The developed coatings demonstrated promising physicochemical properties, bonding performance, wear resistance, and sustained remineralizing ion release, supporting their potential application as therapeutic surface coatings for provisional restorations. Full article

This study investigated the biosynthesis of magnetite nanoparticles mediated by chia mucilage (CM-Fe₃O₄ NPs) and their application in the co-encapsulation of Lactobacillus rhamnosus GG (LGG) using spray drying. CM-Fe₃O₄ NPs were synthesized by combining CM extract with iron salts, in which hydroxyl and carbonyl groups of CM acted as natural ligands for Fe²⁺/Fe³⁺ ions. A response surface design was applied to optimize synthesis parameters, focusing on size distribution and zeta potential, and confirming the influence of pH on colloidal stability. Characterization by FE-SEM, DLS, XRD, UV-Vis, and FTIR revealed spherical particles with an inorganic core (50–300 nm) and a hydrated organic coating (600–900 nm), consistent with a spinel structure functionalized by CM. Spray-drying encapsulation tests showed that incorporating CM-Fe₃O₄ NPs did not compromise bacterial viability, maintaining optimal moisture content and survival. Growth curves and confocal microscopy corroborated the physiological compatibility of the nanoparticles, with no alterations in LGG morphology or growth dynamics. Under simulated gastrointestinal conditions, co-encapsulated microcapsules exhibited slightly improved survival in the gastric phase and significantly greater viability in the initial intestinal phase. These results suggest that CM-Fe₃O₄ NPs modulate matrix degradation and promote controlled release, ensuring therapeutic concentrations of LGG in the intestine. Overall, the CM-Fe₃O₄ nanocomposite system integrates the protective properties of biopolymers with the functional advantages of iron nanoparticles, offering dual functionality: probiotic stabilization and potential iron supplementation. This innovative, food-grade approach supports the development of next-generation functional foods with combined therapeutic and nutritional benefits. Full article

Iron oxide nanoparticles have emerged as multifunctional compounds with prominent potential in cancer theranostics, particularly in photothermal therapy (PTT) and photodynamic therapy (PDT). Their unique electronic and crystal structures, such as the dispersion of Fe²⁺ and Fe³⁺ ions and d-orbital splitting, contribute to their magnetic and catalytic properties. In PTT, Fe₃O₄ nanoparticles exhibit moderate near-infrared (NIR) absorption and photothermal conversion efficiency, which can be enhanced through adjustments in particle size, surface modification, and combinations with other components. In PDT, Fe₃O₄ nanoparticles demonstrate intrinsic peroxidase-like catalytic activity, facilitating Fenton and photo-Fenton reactions that generate reactive oxygen species (ROS), including hydroxyl radicals (^•OH), thereby amplifying oxidative stress in cancer cells. These nanoparticles can also function as carriers for photosensitisers (PS), promoting targeted delivery and enhanced ROS generation. Multifunctional nanomaterials that integrate Fe₃O₄ with other therapeutic agents and targeting ligands have demonstrated synergistic antitumour effects through amplified photothermal, photodynamic, chemodynamic, and chemotherapeutic mechanisms. Despite certain drawbacks, such as relatively low NIR absorption and challenges in optimising delivery and light activation, ongoing improvements in Fe₃O₄-based nanoplatforms present significant potential for enhancing treatment outcomes and the precision of cancer therapy. This article systematically explores the synergistic role of Fe₃O₄ nanoparticles in PTT and PDT, encompassing their magnetic and catalytic characteristics. Additionally, it focuses on multifunctional hybrid nanoplatforms that combine Fe₃O₄ with targeting or imaging agents, highlighting their potential to enhance therapeutic precision. Full article