Search Results (53)

Predicting academic performance in face-to-face computing and software engineering courses is hindered by the limited availability of fine-grained process data. This study proposes STEAP, a camera-based static–temporal fusion framework that integrates longitudinal classroom behavior sensing with conventional educational records. Classroom videos from 375 undergraduates enrolled in four computing-related courses were collected over nine teaching weeks. Camera-derived observable behaviors were organized into student-level weekly sequences and transformed into outcome-independent longitudinal representations. Multiple machine-learning classifiers were subsequently applied to predict students’ academic performance. Checkpoint-specific predictions were conducted at Weeks 3, 6, and 9, with each prediction using only the classroom behavioral information available up to the corresponding time point. Using the complete nine-week Temporal representation together with the pre-course Background variables, XGBoost achieved the strongest classification performance among the evaluated models, with an Accuracy of 0.867, a Macro F1 of 0.862, and an At-risk Recall of 0.924. The checkpoint analyses further indicated that classroom behavioral information collected during the early course stage already provided useful predictive information without incorporating behavioral observations from subsequent weeks. After further integrating pre-course background variables and regular assessment information, the final fusion model achieved an Accuracy of 0.896 and a Macro F1 of 0.895. Overall, longitudinal camera-derived classroom behavior provides complementary predictive information beyond conventional educational information and supports the feasibility of earlier academic-risk identification at different course checkpoints. Full article

Growth and body conformation traits are key determinants of meat production efficiency and economic performance in sheep. However, the genetic architecture underlying these complex traits remains incompletely understood, particularly across multi-breed populations. In this study, we performed a genome-wide association study (GWAS) for seven growth and developmental traits in a combined population of 401 sheep, including Qira Black, Kyrgyz, Dorset × Hu crossbred, and Suffolk × Karakul crossbred sheep. After genotype harmonization and quality control, 47,674 autosomal SNPs were retained for analysis. Population structure was assessed using principal component analysis, and association testing was conducted using a mixed linear model incorporating breed, principal components, and a kinship matrix. A total of 44 independent loci were detected at a nominal significance threshold, encompassing 112 candidate genes. The strongest association was identified for cannon bone circumference near RPS6KA5 (Chr7; p = 1.40 × 10⁻⁷). Several biologically relevant genes involved in osteogenesis, cartilage development, and metabolic regulation were detected, including STEAP3, SLC26A2, PPARGC1B, COL11A1, CALN1, and CITED2. Two genomic regions exhibited pleiotropic effects, which were identified as being associated with multiple traits, suggesting shared genetic regulation of correlated skeletal characteristics. These findings are consistent with a polygenic architecture underlying growth trait in sheep and highlight candidate genomic regions potentially involved in skeletal development and body conformation. Although further validation is required, the identified loci provide preliminary evidence for regions that may influence growth-related phenotypes and offer a reference for future molecular breeding efforts in indigenous and crossbred sheep populations. Full article

Nonylphenol (NP), a typical emerging pollutant, is widely detected in water bodies, yet its hepatotoxic mechanisms and mitigation strategies remain underexplored. This study evaluated the protective effects of a mixed probiotic (Lactobacillus acidophilus and Bacillus subtilis) against NP-induced hepatotoxicity in Silurus meridionalis by integrating transcriptomic and metabolomic analyses, with validation by RT-qPCR and ELISA. The results showed that NP exposure disrupted the arachidonic acid (AA) pathway (activating pro-inflammatory COX and LOX pathways while the suppressing anti-inflammatory CYP450 branch), promoted ferroptosis via iron dyshomeostasis and oxidative damage, and impaired triglyceride (TG) synthesis. Probiotic pretreatment reversed these toxic effects by modulating AA metabolism, suppressing COX (ptgs2a↓ → PGE₂↓) and LOX (alox12↓ → MDA↓) pathways, while upregulating the CYP450 pathway (cyp2j↑ → 11,12-EET↑). Probiotics also enhanced Fe³⁺ sequestration (steap4↑) and antioxidant defense (CAT↑, gpx4a↑), limiting Fenton reaction-mediated oxidative injury, and restored hepatic TG synthesis through upregulation of the DHAP-to-TG cascade (DHAP—(gpd1b↑) → G3P↑—(gpat3↑) → LPA—(agpat6↑) → PA—(plpp7↑) → DAG↑—(dgat2↑) → TG↑). These findings suggest that NP induces hepatotoxicity in S. meridionalis, involving ferroptosis, AA metabolism disruption and impaired TG synthesis as interconnected pathological events. Probiotics likely counteract this toxicity through systemic metabolic reprogramming. Collectively, these findings elucidate the hepatotoxic mechanisms of NP in S. meridionalis and offer toxicological data for its risk assessment, supporting the potential of probiotic-based strategies to mitigate emerging pollutant impacts in aquatic organisms. Full article

Background: Antibody-drug conjugates (ADCs) are gaining rapidly expanding clinical utility, with a growing number of approved indications across compounds that differ in target antigen, payload mechanism, and linker design. However, treatment response remains heterogeneous, and predictive biomarkers to identify patients most likely to benefit are limited. Given that ADC efficacy depends on sufficient target antigen expression and distribution across tumor lesions, positron emission tomography (PET) imaging offers a unique opportunity to non-invasively assess whole-body target availability. We therefore conducted a systematic literature review to evaluate the relationship between PET-measured tumor antigen expression and the therapeutic response to ADCs targeting the same antigen. Method: A systematic comprehensive search of PubMed, EMBASE and Web of Science databases was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, using terms related to targeted PET, ADC treatment and response assessment. Article screening, eligibility assessment, and data extraction were performed independently using predefined criteria by two reviewers. Disagreements were resolved by consensus. Results: A total of 5628 records were identified. After removing duplicates, 4323 records were screened by title and abstract. Fifty-eight underwent full-text review and seven were included in the final review. Four trials investigated human epidermal growth factor receptor 2 (HER2)-targeted therapy, one Nectin-4, one mesothelin and one STEAP1. In all HER2- and Nectin-4-related trials, patients with a higher uptake on targeted PET had a higher probability of responding to targeted treatment. Included trials were generally small and had a moderate risk of bias. Conclusion: Targeted PET imaging showed potential to predict treatment response in trials evaluating clinically active agents. Additional clinical trials across a broader range of targets, along with standardized acquisition protocols and harmonized study designs, are needed to enable the integration of this technique into clinical practice and ultimately translate its benefits to patients. Full article

Background: Polycystic ovary syndrome (PCOS) is a frequently encountered endocrine disturbance with a still poorly defined etiology that arises in women during their reproductive years. Increased apoptosis of granulosa cells has been identified as one of the key factors contributing to abnormal follicular development. This study aimed to elucidate the role of six-transmembrane epithelial antigen of prostate 4 (STEAP4) in granulosa cell function using in vitro and in vivo models relevant to PCOS. Methods: We treated KGN cells (a human granulosa-like cell line) and C57BL/6 mice with dehydroepiandrosterone (DHEA) to establish experimental models mimicking PCOS features. STEAP4 expression was assessed by qRT–PCR, Western blot, and immunohistochemistry. Proliferative capacity and apoptotic rates were gauged with CCK-8 assays, EdU labeling, and flow cytometry. The regulatory mechanisms were investigated through immunofluorescence staining for nuclear factor erythroid–2–related factor 2 (Nrf2) nuclear translocation and immunoprecipitation assays for HIF-1α ubiquitination. Results: Exposure to androgen markedly raised both STEAP4 transcript and protein abundance in KGN cells as well as in PCOS model mice. STEAP4 knockdown resulted in increased proliferation and reduced apoptosis in DHEA–treated KGN cells. Mechanistically, STEAP4 enhanced reactive oxygen species levels, promoted Nrf2 nuclear translocation, and stabilized HIF–1α protein by reducing its ubiquitination, leading to increased TERT expression and subsequent TP53 pathway activation. In vivo, STEAP4 silencing significantly alleviated hormonal imbalances, estrous cycle disorders, and reduced oxidative stress levels in ovarian tissue of DHEA-induced PCOS–like mice. Conclusions: Taken together, evidence from these experimental models indicates that STEAP4 shapes oxidative stress and granulosa cell apoptosis by operating through the ROS–TERT–TP53 axis. The data point to a possible contribution of STEAP4 to PCOS pathogenesis and mark it as a candidate therapeutic target that merits additional clinical study. Full article

To identify candidate genes associated with skin tissue responses in Hu sheep raised under different regional rearing environments and to preliminarily explore their potential relevance to low-temperature-related environmental responses, this study used 1-year-old female Hu sheep raised in Anhui and Xinjiang as the experimental animals. Skin tissues were collected from the left scapular region, and their transcriptomic profiles were characterized by integrating histological analysis, RNA sequencing (RNA-seq), differential expression analysis, functional enrichment analysis, protein–protein interaction (PPI) network construction, and RT-qPCR validation. The results showed significant differences between the two groups in body weight, body length, body height, cannon circumference, rectal temperature, and ear temperature. Hematoxylin and eosin (H&E) staining indicated that the Xinjiang group exhibited a denser distribution of hair follicles, a relatively thicker dermis, and a more compact arrangement of collagen fibers, suggesting enhanced insulation-related skin characteristics. Transcriptome sequencing identified 295 differentially expressed genes (DEGs), including 193 upregulated and 102 downregulated genes. GO and KEGG enrichment analyses showed that these DEGs were mainly involved in immune and inflammatory responses, redox processes, extracellular matrix remodeling, and lipid and energy metabolism-related pathways, with significant enrichment in cytokine–cytokine receptor interaction, the chemokine signaling pathway, the NF-κB signaling pathway, glutathione metabolism, and drug metabolism–cytochrome P450. By further integrating PPI network analysis and functional annotation, CXCL13, CCL2, FGF21, GPX3, CYP1A1, HSD11B1, CDO1, and STEAP4 were identified as candidate genes. RT-qPCR results showed that the expression trends of the selected genes were generally consistent with the RNA-seq results. Overall, this study revealed differences in phenotypic traits, skin histological structure, and transcriptomic characteristics between Hu sheep raised in different regions, providing preliminary molecular clues potentially associated with low-temperature-related environmental responses. Given the differences in geographic origin and rearing environments between the two groups, the findings should be interpreted as associative evidence of skin transcriptomic responses in Hu sheep under different environmental conditions—rather than as direct causal evidence that low temperature alone drove these transcriptomic differences. Full article

Glioblastoma (GBM) is characterized by hypoxia-driven metabolic adaptation and profound therapeutic resistance. Ferroptosis, an iron-dependent lipid peroxidation-related cell death process, has emerged as a potential vulnerability; however, its relationship with hypoxia signaling remains incompletely defined. In this study, we performed integrative transcriptomic and single-cell RNA sequencing analyses to investigate the relationship between hypoxia signaling and ferroptosis-related gene signatures in GBM. Intersection analysis of hypoxia-associated differentially expressed genes and curated ferroptosis-related gene sets identified 29 core candidate genes. FerroScore stratification revealed that tumors with higher ferroptosis-related transcriptional signatures were significantly associated with poor overall survival. Among these genes, HILPDA emerged as a hypoxia-associated gene consistently linked to ferroptosis-related gene expression patterns and immune-related transcriptional programs. HILPDA expression showed significant correlations with iron-ROS axis components, including HMOX1, NOX4, and STEAP3, and was associated with immune microenvironment changes characterized by T cell depletion and inflammatory infiltration. Single-cell RNA-seq analysis further supported the cellular-level association between HILPDA expression and hypoxia-related transcriptional states. Structural equation modeling suggested that the relationship between HILPDA expression and ferroptosis-related gene signatures may be mediated through hypoxia-related pathways. Collectively, these findings indicate a transcriptomic association between hypoxia signaling and ferroptosis-related gene signatures in GBM and identify HILPDA as a candidate gene associated with this axis. Full article

Background: T-cell-engaging bispecific antibodies (TCEs) have transformed haematological malignancy treatment (blinatumomab > 40% complete remission), yet solid tumour efficacy remains limited (<15% response rates) due to antigen heterogeneity, immunosuppressive microenvironments, and T-cell dysfunction. Systematic molecular engineering, biomarker-driven patient selection, and rational tumour microenvironment modulation are now collectively transforming TCEs from experimental agents into an adaptable platform therapy for solid tumours. Methods: Review of 55 phase I–III trials of CD3-based TCEs in solid tumours, including tarlatamab (DLL3-targeted, small-cell lung cancer) and xaluritamig (STEAP1-targeted, prostate cancer). Analysis of next-generation engineering strategies and resistance mechanisms via genomic and immunohistochemical data. Result: Response rates now approach ~40% in selected settings, marking an inflection point. In extensive-stage small-cell lung cancer, tarlatamab achieved ~40% responses with definitive survival benefit (phase III HR 0.60, 95% CI 0.47–0.77; p < 0.001; median OS 13.6 months). In metastatic castration-resistant prostate cancer, xaluritamig produced ~41% responses in heavily pretreated patients. Step-up dosing reduced severe cytokine release syndrome to <1% (as low as 0.6% with teclistamab), enabling outpatient administration. Neurological adverse events require monitoring but are less frequent than with cellular therapies. Together these results mark a decisive transition from proof-of-concept to clinically validated platform therapy. Discussion: Three resistance mechanisms limit durability: (i) antigen heterogeneity (28–60% of progressors develop antigen-negative subclones); (ii) immunosuppressive microenvironments (stromal barriers, myeloid-derived suppressor cells, hypoxia); (iii) T-cell exhaustion (PD-1/TIM-3/LAG-3 co-expression). Conclusions: Next-generation TCE platforms integrating conditional activation, cytokine payloads, and checkpoint modulation—deployed with biomarker-guided selection and TME-modulating combinations—represent a transformative therapeutic strategy. With tarlatamab’s phase III survival benefit establishing clinical proof-of-concept, and pivotal trials underway for xaluritamig and next-generation agents, TCEs are positioned to become standard-of-care platform therapies in biomarker-defined solid tumours by 2028–2030. Full article

Background/Objectives: Ferroptosis, an iron-dependent form of regulated cell death defined by lipid peroxidation, has been extensively studied in cancer and neurodegeneration, but its contribution to erythropoiesis remains poorly understood. Methods: In this study, we investigated the expression of ferroptosis-related genes during HMBA-induced differentiation of murine erythroleukemia (MEL) cells and further assessed the effects of the ferroptosis inducer erastin in this model system. Results: HMBA treatment was accompanied by upregulation of ferroptosis-inducing genes (Atf3, Por, Tfrc, Slc11a2) and downregulation of inhibitory genes (Dhfr, Aifm2, Flvcr1, Nfe2l2, Slc3a2, Slc7a11), while Gpx4 levels increased. Erastin exposure identified 5 μM as the optimal concentration, which resulted in a significant reduction of Steap3 transcripts, an increase in Hbb expression, and an increased accumulation of differentiated cells in culture, along with mild cytotoxicity. To be noted that at the protein level, erastin induced a ~10% decrease in STEAP3 and a 1.5-fold increase in β-globin homo- or hetero-dimers. Ferroptosis markers confirmed erastin activity, with Fsp1 to be downregulated and Slc7a11, ferroportin, and the transferrin receptor upregulated. Importantly, erastin also enhanced apoptotic responses, as indicated by increased levels of active caspase-3 (~40%) and reduced cellular proliferation rate (Ki-67, ~35%), suggesting overlap between ferroptotic and apoptotic pathways. Conclusions: Collectively, these findings indicate that erastin modulates erythroid maturation by repressing Steap3 (Six-transmembrane epithelial antigen of prostate 3) and enhancing Hbb expression, yet its differentiation inducing potential is counterbalanced by concurrent apoptosis activation. Overall, our results support a role of ferroptosis in erythroid maturation by linking iron metabolism, regulated cell death, and erythropoiesis, a fact of pharmacological and therapeutic relevance too. Full article

Background/Objectives: The aim of the current study was to investigate the mechanistic hepatoprotective efficacy of selenium (SE) and chitosan-coated selenium nanoparticles (CS-SENPs) using a rat model induced by lipopolysaccharide (LPS). Methods: CS-SENP was prepared and characterized for particle size, polydispersity index (PDI), zeta potential, transmission electron microscope (TEM), and Fourier transform infrared spectroscopy (FTIR). Male albino rats (n = 40) were divided into four groups: control, LPS, SE, and CS-SENP. SE and CS-SENPs (5 mg/kg orally for 14 days) were given before LPS injection. Tissue architecture was assessed using histopathological analysis. HSP-47 and STEAP-3 protein expression levels were measured using ELISA, and oxidative stress markers were quantitatively evaluated. The expression of HO-1, TLR-4, STAT-3, TRAF-6, and IL-17A was measured using immunohistochemical analysis. Furthermore, HSP-90 expression was evaluated by immunofluorescence labeling. Results: CS-SENP characterization revealed uniform (PDI = 0.125 ± 0.04) nanoparticle size (108.54 ± 2.24 nm), with high zeta potential (+63.92 ± 6.287 mV), attributed to the CS layer, which was confirmed by FTIR and TEM as an electron-lucent halo enveloping the individual SENP cores. CS-SENPs significantly reduced lipid peroxidation (MDA) and restored glutathione (GSH) more effectively than SE. CS-SENPs improved redox (upregulated HO-1) and iron balance (downregulated STEAP-3), and also increased the anti-inflammatory effect (suppressed TLR-4, IL-17A, TRAF-6, and STAT-3). CS-SENPs showed superior antifibrotic efficacy (suppresses stress proteins, HSP-47 and HSP-90). Rats treated with CS-SENPs had nearly normal liver structure. Conclusions: The results concluded that CS-SENPs had superior and multi-targeted hepatoprotection against LPS-induced liver damage. Full article

Background/Objectives: The micronutrient iron is closely connected to inflammation and is among the complex factors contributing to beta-cell failure in diabetes. High levels of dietary iron increase the risk of developing type 2 diabetes, and excessive iron uptake by beta-cells can cause oxidative stress and inhibit function. Elevated levels of proinflammatory cytokines in obese individuals, such as interleukin (IL)-1beta and IL-6, increase the risk of developing type 2 diabetes, and there is evidence that these low levels of circulating cytokines can lead to islet dysfunction. Methods: In this study, gene microarray and other data were analyzed for expression differences in islets treated for 48 h with 10 pg/mL IL-1beta + 20 pg/mL IL-6 as a model of low-grade inflammation versus untreated. Results: Three iron-associated genes were among the most cytokine-sensitive in the mouse genome: Hamp, Steap4, and Lcn2. These proteins are all involved with increasing/retaining cellular iron. We hypothesized that increased cellular iron would lead to increased susceptibility to ferroptosis. Surprisingly, 24 h pre-exposure to low-grade inflammation, which upregulates this iron-gene network, prevented subsequent erastin-induced ferroptosis. We also found that Steap4 overexpression reduced islet dysfunction caused by high-dose proinflammatory cytokines (10× low-dose), suggesting an overall protective effect. Steap4 overexpression also upregulated Hamp and Lcn2, suggesting Steap4 regulates these cytokine-sensitive iron genes.; in contrast, ferritin and ferroportin gene expression, which are not sensitive to cytokines, were unchanged. Conclusions: These data suggest an inflammation-induced network of genes involved in cellular iron uptake and retention plays a protective role in islets against oxidative stress and ferroptosis. Full article

Lipopolysaccharide (LPS) triggers oxidative damage in sheep hepatocytes, linked to ferroptosis. Ferulic acid (FA) is known for its antioxidative properties, but its protective role against LPS via ferroptosis regulation was unclear. The objective of this research is to explore the protective role of FA in mitigating LPS-induced oxidative stress in sheep hepatocytes. The experimental setup consisted of three groups: a control group, an LPS group treated with 10 µg/mL of LPS, and FA group that received both 10 µg/mL of LPS and 750 µg/mL of FA. We found that FA treatment decreased in contents of MDA and LDH. Metabolomics revealed that LPS affected glycerophospholipid metabolism, unsaturated fatty acids biosynthesis, ferroptosis, and arachidonic acid metabolism mainly by reducing the level of PUFAs and LPC in the hepatocyte supernatant, while FA affected glutathione metabolism by increasing L-cysteine, L-ornithine, L-glutamic acid, and L-glutamine. Moreover, transcriptomics demonstrated that the comparison of LPS and control groups were mainly enriched in arachidonic acid metabolism, glycerophospholipid metabolism, and ferroptosis, the comparison of FA and LPS groups was mainly enriched in glutathione metabolism. The results further confirmed the findings in the metabolomics and transcriptomics analyses, showing that LPS treatment upregulated the mRNA expression of ACSL4, LPCAT3, ALOX15, STEAP3, GPX4, GCLC, and GCL in hepatocytes, while reducing GSH and GR levels. In contrast, FA intervention attenuated LPS-induced iron overload by decreasing Fe²⁺ accumulation and suppressing the mRNA expression of ACSL4, LPCAT3, STEAP3, and ALOX15. Furthermore, FA enhanced the expression of GPX4, GCLC, GCLM, and restored GSH content in LPS-exposed hepatocytes. The above results demonstrated that the protective effect of FA on LPS-induced oxidative damage in the sheep hepatocytes was achieved by activating the GSH-GPX4 pathway and inhibiting lipid metabolism-mediated ferroptosis. Full article

Basal cell carcinoma (BCC), the most common skin cancer, is primarily driven by Hedgehog (Hh) and TP53 pathway alterations. Although additional pathways were implicated, the mutational landscape in Asian populations, particularly Koreans, remains underexplored. We performed whole-exome sequencing of BCC tumor tissues from Korean patients and analyzed mutations in 11 established BCC driver genes (PTCH1, SMO, GLI1, TP53, CSMD1/2, NOTCH1/2, ITIH2, DPP10, and STEAP4). Mutational profiles were compared with Caucasian cohort profiles to identify ethnicity-specific variants. Ultraviolet (UV)-exposed and non-UV-exposed tumor sites were compared; genes unique to non-UV-exposed tumors were further analyzed with protein–protein interaction analysis. BCCs in Koreans exhibited distinct features, including fewer truncating and more intronic variants compared to Caucasians. Korean-specific mutations in SMO, PTCH1, TP53, and NOTCH2 overlapped with oncogenic gain-of-function/loss-of-function (GOF/LOF) variants annotated in OncoKB, with some occurring at hotspot sites. BCCs in non-exposed areas showed recurrent mutations in CSMD1, PTCH1, and NOTCH1, suggesting a UV-independent mechanism. Novel mutations in TAS1R2 and ADCY10 were exclusive to non-exposed BCCs, with protein–protein interaction analysis linking them to TP53 and NOTCH2. We found unique ethnic-specific and UV-independent mutational profiles of BCCs in Koreans. TAS1R2 and ADCY10 may contribute to tumorigenesis of BCC in non-exposed areas, supporting the need for population-specific precision oncology. Full article

Advanced prostate cancer (PCa) remains lethal despite standard therapies, and immune checkpoint inhibitors offer limited benefit in its “immune-cold” microenvironment. T-cell engagers (TCEs)—bispecific antibodies linking CD3 on T-cells to tumor-associated antigens (TAAs)—provide potent, MHC-independent cytotoxicity, overcoming a key resistance mechanism. While early PSMA-targeted TCEs established proof-of-concept, recent data, notably for six transmembrane epithelial antigen of the prostate 1 (STEAP1)-targeting agents like Xaluritamig, demonstrate more substantial objective responses, highlighting progress through improved target selection and molecular design. This review synthesizes the evolving landscape of TCEs targeting PSMA, STEAP1, and DLL3 in PCa. We critically evaluate emerging clinical evidence, arguing that realizing the significant therapeutic potential of TCEs requires overcoming key challenges, including cytokine release syndrome (CRS), limited response durability, and antigen escape. We contend that future success hinges on sophisticated engineering strategies (e.g., affinity tuning, masking, multispecific constructs) and rationally designed combination therapies tailored to disease-specific hurdles. Strategies for toxicity mitigation, the crucial role of biomarker-driven patient selection, and potential integration with existing treatments are also discussed. Accumulating evidence supports TCEs becoming a new therapeutic pillar for advanced PCa, but achieving this demands sustained innovation focused on optimizing efficacy and safety. This review critically connects molecular engineering advancements with clinical realities and future imperatives. Full article

The myogenic differentiation of muscle satellite cells (MuSCs) is an important biological process that plays a key role in the regeneration and repair of skeletal muscles. However, the mechanisms regulating myoblast myogenesis require further investigation. In this study, we found that STEAP3 is involved in myogenic differentiation based on the Yunan black pig MuSCs model in vitro using cell transfection and other methods. Furthermore, the expression of myogenic differentiation marker genes MyoG and MyoD and the number of myotubes formed by the differentiation of cells from the si-STEAP3 treated group were significantly decreased but increased in the STEAP3 overexpression group compared to that in the control group. STEAP3 played a role in iron ion metabolism, affecting myogenic differentiation via the uptake of iron ions and enhancing IRP-IRE homeostasis. STEAP3 also activated the PI3K/AKT pathway, thus promoting myoblast differentiation of Yunan black pig MuSCs. The results of this study showed that STEAP3 overexpression increased intracellular iron ion content and activated the homeostatic IRP-IRE system to regulate intracellular iron ion metabolism. Full article