Search Results (1,021)

Background: The exocyst complex, a conserved hetero-octameric complex including the EXO70 subunit, is a pivotal regulator of various cellular and developmental processes in plants. Among the diverse EXO70 isoforms, the specific function of EXO70E2—a primary organizer of exocyst-positive organelles (EXPOs)—remains to be fully elucidated. Methods: Here, we investigated the functional impact of constitutive EXO70E2 overexpression in Arabidopsis thaliana. Results: We observe that EXO70E2 overexpression leads to severe etiolation and dwarfism, accompanied by dose-dependent inhibition of primary root elongation. The YFP-labeled EXO70E2 localizes to distinct punctate structures. Histochemical analysis shows EXO70E2 expression in root tips and leaf vasculature, and its promoter activity is strongly induced by the salicylic acid analog INA and pathogen infection. Further function dissection demonstrates that EXO70E2-overexpressing plants exhibit enhanced susceptibility to the necrotrophic fungus Botrytis cinerea, manifested as larger lesions, accelerated host cell death, and increased fungal biomass. Conclusions: Our findings position EXO70E2 as a key negative regulator of plant development and defense outcomes, which may play a role in the balance between growth and immunity. Full article

In this work, we analyzed the ability to incorporate 8-oxo-dATP by several human DNA polymerases: replicative Pol ε (exo-) from Family B; base excision repair (BER) enzymes Pol β and Pol λ from Family X; and translesion Pol η, Pol ι, and Pol κ from Family Y. We demonstrated that human DNA polymerases differ in their abilities to discriminate against 8-oxo-dATP. Among the tested DNA polymerases, Pol λ exhibited the worst ability to discriminate against 8-oxo-dATP opposite template T on DNA substrates with a protruding single-stranded 5′-end and a double-stranded DNA with a 1 nt gap. Pol β and DNA polymerases of Family Y showed relatively high accuracy. Pol η demonstrated the most effective discrimination against 8-oxo-dATP on templates T and G. Pol ι exclusively incorporated 8-oxo-dATP opposite template G but not T. Unexpectedly, the catalytic subunit of high-fidelity Pol ε (exo-) incorporated 8-oxo-dATP opposite templates T and G with higher efficiency compared with the error-prone polymerases of Family Y and Pol β. While the structures of human polymerases with incoming 8-oxo-dATP are not available, we speculate on a possible mechanism of 8-oxo-dATP discrimination. Full article

Severe skeletal muscle injury in dogs can result in muscle atrophy, fibrotic remodeling, and fat accumulation, leading to skeletal muscle dysfunction and impaired quality of life. However, there is currently no effective treatment available. This study aims to investigate the potential of canine adipose mesenchymal stem cell-derived exosomes (cADMSC-Exos) as a novel acellular therapy for the repair of muscle atrophy and injury. cADMSCs and their derived exosomes were isolated and characterized. A dexamethasone-induced C2C12 myotube atrophy model was established to evaluate the effects of cADMSC-Exos on muscle atrophy by assessing myotube morphology and the expression of atrophy-related factors. Subsequently, a glycerol-induced mouse muscle injury model was constructed. Through histological analysis and Western blot, the efficacy and safety of cADMSC-Exos in vivo were systematically evaluated. Results indicated that cADMSC-Exos demonstrated significant anti-atrophic activity in both two models, ameliorating skeletal muscle atrophy and the upregulation of muscle RING finger 1 (MuRF1) and muscle atrophy F-box (Atrogin-1) (p < 0.05), consistent with morphological alterations. Moreover, cADMSC-Exos markedly alleviated fibrosis and fatty infiltration in injured muscle tissue (p < 0.0001). Overall, these findings indicate that cADMSC-Exos promote muscle repair and attenuate pathological remodeling by modulating the local microenvironment and protein expression, highlighting their potential as a therapeutic strategy for muscular disorders. Full article

The field of extracellular vesicle (EV) research offers a compelling example of a biological concept refined through continuous methodological innovation. This review traces the historical trajectory of the discipline chronologically, beginning with early observations in haemostasis, from Malpighi’s descriptions of blood clots and Chargaff and West’s identification of a procoagulant sedimentable plasma fraction, to Wolf’s “platelet dust,” Crawford’s microparticles characterised by electron microscopy, and the seminal work by Stahl and Johnstone demonstrating regulated vesicle biogenesis during reticulocyte maturation via multivesicular bodies. We highlight a pivotal conceptual shift, from viewing EVs as cellular debris to recognising them as regulated “communicasomes,” catalysed by Raposo’s discovery of antigen-presenting exosomes and subsequent evidence for EV-mediated transfer of functional receptors and nucleic acids, including the influential and sometimes debated model proposed by Ratajczak. By integrating findings from matrix vesicles, plant-derived vesicles, and diverse tissue contexts, we frame EV release as an evolutionarily conserved process with profound implications for immunity, regeneration, oncology, and cardiovascular pathology. A second central aim of this review is practical and methodological. We map how the expansion of biological claims has driven urgent standardisation efforts, notably through the establishment of the International Society for Extracellular Vesicles (ISEV) and the successive MISEV guidelines (2014, 2018, 2023). These are complemented by community resources such as EV-TRACK, MIFlowCyt-EV, and the databases ExoCarta and Vesiclepedia. We summarise core experimental choices across isolation and characterisation techniques, including ultracentrifugation, size exclusion chromatography, density gradients, flow cytometry, nanoparticle tracking analysis, and electron microscopy, while outlining persistent bottlenecks in purity, standardised nomenclature, and experimental reproducibility. Finally, we provide concise biographical sketches of key contributors and an overview of major EV-focused journals and ISEV meetings that anchor consensus-building and the translation of fundamental knowledge into clinical and industrial applications. Full article

Forestry, nursery, and planting tasks involve repetitive trunk flexion, squatting, and kneeling, as well as manual handling, increasing musculoskeletal load, and the need for mobility-related safety measures. Passive exoskeletons could mitigate postural exposure and reduce the overall body workload. We conducted a preliminary study (n = 14) to test the feasibility of a protocol and estimated model- and task-specific trends during standardized simulated nursery activities in a laboratory setting. Participants simulated planting and seeding tasks (loads of 0.5–2 kg) and material handling and preparation tasks (loads of 5–15 kg) without an exoskeleton (No-EXO) and with three passive models (EXO 1–EXO 3). EXO 3 was excluded from the planting tasks for feasibility reasons. Whole-body kinematics were recorded using an IMU-based motion capture system and converted into time-based ergonomic exposure outcomes (OWAS and RULA). Physiological load was monitored via heart-rate (HR) measurements. Compared to the No-EXO condition, exoskeleton use shifted posture exposure towards lower-risk categories. The largest improvements were observed with EXO 2 and EXO 3 during material handling (OWAS: −18%/−20%; RULA action-level reduction: −25%/−39%) and with EXO 2 during planting/seeding (OWAS: −15%; RULA: −26%). HR_max did not increase across tasks or conditions and HR tended not to rise with higher workload when exoskeletons were used. Overall, the results suggest positive ergonomic and workload trends related to the model and tasks. Field validation on uneven terrain with full personal protective equipment and harness integration is needed to confirm usability and support and to define implementation requirements (fit, compatibility with PPE, and safe-use conditions). Full article

Background/Objectives: Astrocytes play a critical role in maintaining brain homeostasis and are increasingly recognized as active contributors to neurodegenerative processes. Metabolic dysfunction in astrocytes has been implicated in the onset and progression of Alzheimer’s disease (AD), yet the underlying metabolic alterations remain poorly characterized. Methods: We used an optimized protocol for untargeted metabolomic profiling of both intracellular and extracellular compartments of primary human astrocytes derived from AD patients and healthy subjects (HS) using ¹H nuclear magnetic resonance (NMR) spectroscopy. Cells were treated with oligomeric Aβ_1-42 to model pathological conditions. Results: Aβ_1-42 treatment induced intracellular metabolic alterations in both AD and HS astrocytes, including a consistent reduction in phosphocreatine, potentially indicating impaired energy-buffering capacity. Notably, a decrease in β-alanine was observed only in AD astrocytes, suggesting alterations in carnosine-related antioxidant defence. Analysis of conditioned media revealed differential responses between groups: AD astrocytes showed increased extracellular levels of 2-oxoglutarate, citrate, and glycine, whereas HS astrocytes exhibited reduced extracellular levels of leucine and isoleucine, suggesting distinct adaptive metabolic responses to Aβ-induced stress. However, none of these differences remained statistically significant after correction for multiple testing. Conclusions: These findings suggest that NMR-based metabolomics can detect subtle metabolic shifts in human astrocyte models of AD and HS exposed to amiloidogenic challenge. Given the limited sample size and the exploratory design adopted, the results should be interpreted as preliminary and require validation in larger, better-matched cohorts. Nevertheless, this study provides a methodological framework and generates biologically plausible hypotheses regarding astrocyte metabolic responses relevant to AD pathophysiology. Full article

Background: Bronchopulmonary dysplasia (BPD) is a common lung disease in premature infants. Hyperoxia-induced oxidative stress and ferroptosis are key pathological mechanisms leading to alveolar epithelial (AT) cell injury and impaired alveolar development. M2 macrophage-derived exosomes (M2-Exo), as intercellular communication carriers, have potential protective effects in regulating oxidative stress-related diseases, but the molecular mechanism by which they exert effects by regulating ferroptosis in BPD remains unclear. Objective: To explore the protective effect of M2-Exo on hyperoxia or inflammation-induced BPD models and clarify its antioxidant mechanism. Method: In vitro AT cell injury models and in vivo BPD models were constructed by hyperoxia or LPS induction. M2-Exo were isolated, identified, and used to intervene in models. Oxidative stress and ferroptosis-related indicators (ROS, MDA, iron accumulation, GPX4), AT cell functional markers (AQP5, SPC), and ZAKα-p38 pathway activation contents were detected. ZAKα overexpression was used to verify pathway dependence. Results: M2-Exo intervention significantly enhanced AT cell viability, upregulated the expression of AQP5 and SPC, and reversed alveolar simplification. Concurrently, it effectively suppressed hyperoxia or LPS-induced oxidative stress and ferroptosis, as evidenced by reduced contents of ROS and MDA, diminished iron accumulation, and GPX4 expression. Mechanistically, M2-Exo significantly inhibited the activation of the ZAKα-p38 pathway, and ZAKα overexpression could antagonize the antioxidant, anti-ferroptotic, and AT cell protective effects of M2-Exo. Conclusions: M2-Exo alleviate AT cell oxidative stress and ferroptosis by inhibiting the ZAKα-p38 pathway, thereby improving hyperoxia or inflammation-induced BPD and providing a new strategy and molecular target for the antioxidant treatment of BPD. Full article

This study identifies electromyography (EMG) features as an alternative to metabolic cost for distinguishing varying levels of movement effort. Data from two experiments was used to analyze the performance of 50 EMG-based features. The first experiment, the Load experiment, involved participants walking with and without carrying loads of 2, 4, and 8 kg, and the second, the Exo experiment, had participants walking with and without varying levels of hip exoskeleton assistance. In the Load experiment, amplitude-based features generally performed well, with Waveform Length (WL) emerging as the top-performing feature achieving a detection rate of 77% when distinguishing between loaded and unloaded conditions in the most challenging 2 kg condition. In contrast, in the Exo experiment, where both increases and decreases in EMG were observed throughout the stride, it failed and mean-based as well as variance-based features performed best and effectively captured fluctuations in muscle activation with a detection rate of up to 71%. This study underscores the importance of selecting EMG features tailored to specific movement tasks and highlights the potential benefits of noise management strategies to improve detection performance for varying levels of movement effort, providing a foundation for EMG-based human-in-the-loop optimization of lower limb exoskeletons. Full article

Pancreatic ductal adenocarcinoma (PDAC) is characterized by immune cell dysfunction and poor prognosis. CD44, a cell surface glycoprotein with multiple splice variants, has been implicated in tumor progression, but its compartment-specific roles in PDAC remain unclear. CD44 standard and variant isoform expression was analyzed in patient-derived lymph nodes (LNs) by quantitative PCR. Immune cell-specific CD44 expression was assessed by flow cytometry in LNs and peripheral blood. Soluble and exosome-associated CD44 (exo-CD44) were measured in plasma. Clinical associations and survival analyses were performed. Transcriptomic, immune infiltration, immune checkpoint, and drug sensitivity analyses were conducted using TCGA-PAAD and pharmacogenomic datasets. CD44 standard isoform expression was unchanged in PDAC LNs, whereas multiple CD44 variant isoforms (v4–v10) were significantly reduced and associated with metastatic disease and poor survival, particularly CD44v5, v6, v7, and v10. CD44 expression was enriched in CD45⁺ immune cells, with highest levels in CD4⁺ T cells in both LNs and blood. Soluble CD44 levels showed no clinical associations. In contrast, exo-CD44 levels were reduced overall in PDAC but increased in patients with distant metastasis, positive resection margins, systemic inflammation, and reduced survival. High CD44 expression was associated with advanced disease, immune cell infiltration, immune checkpoint gene expression, reduced sensitivity to gemcitabine, paclitaxel, rapamycin, and FMK, and distinct CTLA4/PD-L1 checkpoint profiles. CD44 exhibits compartment-specific regulation in PDAC, linking immune remodeling, exosome signaling, and therapeutic resistance to adverse clinical outcome. Full article

The number of pet dogs is increasing, and the number of working dogs (e.g., guide dogs, police dogs) is also gradually increasing. Skin wounds are a common clinical problem in dogs and tend to be more common in the clinic as mechanical wounds. The healing process of skin wounds is often influenced by a variety of factors, including infection, nutritional status, and immune response, while wound healing is more difficult in dogs with diabetes or aging dogs. Mesenchymal stem cells (MSCs) play an important role in skin healing and regeneration with their multidirectional differentiation potential and immunomodulatory function. However, the application of MSCs alone for the treatment of skin wounds may have certain limitations, such as low cell survival and a lack of localization. Therefore, it is important to find methods that can enhance the therapeutic effect of MSCs. Secreted protein acidic and rich in cysteine (SPARC), an extracellular matrix protein widely involved in regulating biological processes such as cell proliferation, migration, and matrix production, may enhance the efficacy of MSCs in skin wound healing. This study aims to systematically evaluate the therapeutic efficacy of SPARC-overexpressing adipose-derived mesenchymal stem cells (ADSCs) in promoting skin wound healing by establishing wound models in normal, diabetic, and aged mice and dogs, thereby validating their potential under diverse physiological and pathological conditions. For in vitro validation, we used hydrogen peroxide (H₂O₂) to induce Human Umbilical Vein Endothelial Cell (HUVEC) and Human Keratinocyte Cell (HaCaT) injury. All animals were randomly assigned to six experimental groups as follows: (1) Model group: Untreated wound (negative control); (2) HY group: Hydrogel alone (vehicle control); (3) Con group: Control-ADSCs (cell control); (4) Con-Exo&HY group: Control-ADSC exosomes in hydrogel; (5) SPARC group: oe-SPARC-ADSCs (treatment); (6) SPARC-Exo&HY group: oe-SPARC-ADSC exosomes in hydrogel (treatment). Separately, HUVEC and HaCaT cells were assigned to four experimental conditions: a blank control group, a model group, a control-ADSC-treated group, and an oe-SPARC-ADSC-treated group. ADSCs modified by SPARC significantly promoted re-epithelialization integrity, collagen deposition, inflammation reduction, angiogenesis, and hair follicle regeneration during wound healing in dog skin. HUVEC and HaCaT cells proliferated after adding oe-SPARC-ADSCs cell supernatant. Meanwhile, quantitative proteomic sequencing data analysis showed that SPARC could promote skin wound healing by enhancing cell adhesion, hyaluronic acid binding, and vascular smooth muscle contraction of ADSCs. Both in vitro cellular assays and in vivo wound-healing models suggest that the combination of SPARC and ADSCs for the treatment of skin wounds has broad application prospects. Full article

Background: Carbapenem-resistant Pseudomonas aeruginosa (CRPA) has been added to the World Health Organization’s list as a high-priority pathogen for which new antibiotics are urgently needed. Herein, we investigated the association between resistance/virulence genes and high-risk CRPA clinical isolates by whole genome sequencing (WGS). Methods: Between 2019 and 2025, twenty-six CRPA strains from patients hospitalized in the “Renato Dulbecco” University Hospital were characterized. WGS analysis was performed using the next generation sequencing (NGS) technique. Multi-locus sequence typing (MLST) prediction was performed. Antibiotic resistance genes were detected using Antibiotic Resistance Gene-ANNOTation, Comprehensive Antibiotic Resistance Database, and ResFinder. Virulence genes were identified by the Virulence Factor Database. Results: The MLST analysis detected 14 different sequence types (ST). The 26 strains exhibited the same resistome profile: aac(3)-Ic, aphA15, catB7, catB10, cmlA, blaCARB, blaVIM-1, and tetG genes. The genes encoding enzymes involved in resistance to chloramphenicol and beta-lactams were found in all isolates using the three databases. Biofilm formation genes, metalloproteinase, chemotaxis, fimbriae, and pyoverdine were identified in all strains. Genes of the type III secretion system exoS, exoT, exoU, and exoY were found in 46.15%, 84.61%, 53.84%, and 84.61% of the strains, respectively. Conclusions: The analysis of the 26 clinical isolates showed high clonal heterogeneity, with a predominance of ST235, a high-risk clone associated with multiple resistances. Interestingly, cefiderocol resistance was carried by 4/8 isolates belonging to the ST235 strain. The surveillance based on resistome and virulome analysis could monitor the dynamic evolution of high priorityhigh-priority pathogens to guide clinical treatment and to adapt healthcare control measures, limiting their spread in the near future. Full article

Breast cancer is the most frequently diagnosed malignancy among women worldwide, with the luminal A subtype being the most prevalent. Several studies have reported a complex interplay between breast cancer cells and the local microbiome; however, the mechanisms by which tumor cell-secreted factors influence bacterial biological properties remain insufficiently explored. In this study, we established an in vitro model that partially recapitulates the luminal A breast cancer microenvironment by exposing three breast-associated bacterial species, Pseudomonas aeruginosa, Enterococcus faecalis, and Escherichia coli, to conditioned media (CM) derived from MCF-7 (tumor) or MCF-10A (non-tumor control) cell lines. A combination of complementary approaches, including ultrastructural morphological assessment, biofilm formation assays, antimicrobial susceptibility testing, and virulence gene abundance profiling by genomic qPCR, was employed to reveal distinct tumor-microbiota interactions. Exposure to MCF-7 CM induced dose-dependent structural alterations in P. aeruginosa and E. faecalis, with pronounced membrane blebbing and structural disruption in E. faecalis. Biofilm formation was differentially modulated in a species- and concentration-dependent manner, with a persistent increase observed in E. coli. Antibiotic susceptibility profiles were selectively altered in E. faecalis, which displayed increased sensitivity to vancomycin, penicillin, and imipenem, along with decreased sensitivity to chloramphenicol. P. aeruginosa exhibited increased sensitivity to imipenem along with reduced sensitivity to meropenem and gentamicin, whereas no significant changes were observed in E. coli. qPCR analyses demonstrated that MCF-7 CM was associated with enrichment of multiple virulence-associated genes (e.g., lasB, exoS, pilB, plcH, fsrC, esp, fimH, and papG), reflecting enhanced pathogenic and adhesive potential. Collectively, these findings suggest that luminal A breast cancer-derived factors can reprogram microbial phenotypes in a species-specific manner, providing mechanistic insight into breast tumor-microbiome crosstalk and a platform to explore microbiome-targeted interventions. Full article

Acute and chronic kidney diseases remain significant challenges in regenerative medicine, with few therapies capable of reversing tissue injury or preventing progression. Bone marrow mesenchymal stem cell-derived exosomes (BM-MSC-Exos) are nanosized vesicles (30–150 nm) that have emerged as multifunctional nanotheranostic platforms, combining targeted therapeutic activity with imaging-enabled monitoring. In renal pathophysiology, BM-MSC-Exos exert anti-inflammatory, anti-fibrotic, angiogenic, and pro-regenerative effects. These actions are mediated by microRNAs, messenger RNAs, mitochondrial regulators, and bioactive proteins that modulate epithelial repair and immune responses. Recent bioengineering advances enable more precise BM-MSC-Exos design, including enrichment with synthetic RNAs or gene-editing components and membrane functionalization to enhance kidney tropism. In parallel, fluorescence, bioluminescence, and nanoparticle-based approaches support in vivo tracking. These tools allow real-time assessment of biodistribution and tubular uptake, strengthening evidence for target engagement. This review synthesizes current knowledge on BM-MSC-Exos in renal repair. We summarize contemporary strategies for cargo and surface engineering, outline imaging methodologies for in vivo tracking, and discuss how administration routes influence renal targeting. We also provide an updated overview of clinical trials evaluating exosomes as therapeutic agents or biomarkers in nephrology. Collectively, engineered BM-MSC-Exos represent a promising and increasingly sophisticated platform for precision-guided kidney therapy, supported by monitoring tools that facilitate preclinical evaluation of biodistribution and efficacy. Full article

Objective: Hepatic ischemia–reperfusion injury (HIRI) is a common pathological condition in liver surgery and transplantation, and cellular pyroptosis plays a key role in its pathogenesis. However, the clinical application of curcumin is limited by its poor water solubility and low bioavailability. This study aims to develop mesenchymal stem cell (MSC)-derived exosomes loaded with curcumin (Exo-Cur). It also investigates the role and mechanism of Exo-Cur in inhibiting HIRI-related cellular pyroptosis. Methods: The preparation of Exo-Cur was optimized using orthogonal experimental design. Its solubility, stability, particle size distribution, and zeta potential were then evaluated. The morphology of Exo-Cur and its uptake in hepatocytes were observed using laser scanning confocal microscopy. The effect of Exo-Cur on HIRI was assessed through hematoxylin and eosin (HE) staining, ALT and AST measurements, TUNEL assay, CCK-8 assay, and lactate dehydrogenase (LDH) assay. Inflammatory cytokine protein levels were quantified by ELISA, and their mRNA expression was assessed by qRT-PCR. Pyroptosis was assessed by Western blot, immunohistochemistry, and flow cytometry. Additionally, protein expression changes in the PI3K/Akt/mTOR signaling pathway were analyzed using Western blot. Results: Orthogonal experiments determined that the optimal preparation method for Exo-Cur involves cell density at 95%, a curcumin concentration of 30 μg/mL, and a co-cultivation time of 12 h. Characterization results showed that Exo-Cur maintained its typical cup-shaped structure as well as stable particle size and zeta potential. Additionally, its water solubility and its stability in vitro were significantly improved compared to free curcumin. Further mechanistic studies indicated that Exo-Cur could ameliorate the abnormal morphology resulting from HIRI-induced hepatocyte pyroptosis, reduce the proportion of pyroptotic cells, and significantly downregulate the expression of NLRP3 inflammasome and downstream pyroptosis-related proteins (ASC, C-Caspase-1, GSDMD-N). Pathway analysis revealed that Exo-Cur activates the PI3K/Akt/mTOR axis, a pathway inhibited by HIRI. Moreover, rapamycin, an inhibitor of this pathway, reverses Exo-Cur’s anti-pyroptosis effect. Conclusions: This study develops an efficient and stable Exo-Cur delivery system, confirming its protective effect against HIRI by activating the PI3K/Akt/mTOR axis and inhibiting NLRP3-mediated cellular pyroptosis. This innovative combination of MSC-derived exosomes combined with curcumin overcomes the limitations in clinical application of curcumin, such as poor bioavailability and stability, and offers a novel nanotherapeutic strategy to treat HIRI clinically. Full article

Androgenetic alopecia (AGA) and telogen effluvium (TE) are common hair loss disorders characterized by dysregulated hair follicle cycling and impaired dermal papilla cell function. Emerging evidence indicates that exosomes are key mediators of intercellular communication, largely through their microRNA (miRNA) cargo. Milk-derived exosomes (Mi-Exos) represent an accessible and biologically active source of regulatory miRNAs with potential relevance for hair disorders. This study evaluated the in vitro effects of bovine milk-derived exosomes (MEV-miRNAs) on human hair follicles. MEV-miRNAs were enriched in miRNA families (Let-7, miR-21, miR-30, miR-200, and miR-148/152) previously implicated in hair follicle regulation. Viability/metabolic activity of hair follicle dermal papilla (HFDP) cells was assessed, and human hair follicles were cultured ex vivo to measure shaft elongation and modulation of the WNT signaling pathway by qRT-PCR. MEV-miRNAs significantly increased HFDP cell viability after 24 h compared with controls. Human hair follicles showed a non-significant trend toward increased elongation following treatment. Gene expression analysis revealed significant up-regulation of key WNT pathway components, including WNT2, WNT5B, WNT10A, WNT11, MMP7, WISP1, and NKD1, indicating modulation of WNT-associated pathways implicated in hair follicle growth and cycling. Overall, MEV-miRNAs exhibit positive modulatory effects on signaling pathways, supporting their potential as a novel therapeutic strategy for AGA and TE. Full article