BMC Cancer. 2025 Jun 5;25(1):1006. doi: 10.1186/s12885-025-14392-6.

ABSTRACT

OBJECTIVE: To create an automated PET/CT segmentation method and radiomics model to forecast Mismatch repair (MMR) and TP53 gene expression in endometrial cancer patients, and to examine the effect of gene expression variability on image texture features.

MATERIALS AND METHODS: We generated two datasets in this retrospective and exploratory study. The first, with 123 histopathologically confirmed patient cases, was used to develop an endometrial cancer segmentation model. The second dataset, including 249 patients for MMR and 179 for TP53 mutation prediction, was derived from PET/CT exams and immunohistochemical analysis. A PET-based Attention-U Net network was used for segmentation, followed by region-growing with co-registered PET and CT images. Feature models were constructed using PET, CT, and combined data, with model selection based on performance comparison.

RESULTS: Our segmentation model achieved 99.99% training accuracy and a dice coefficient of 97.35%, with validation accuracy at 99.93% and a dice coefficient of 84.81%. The combined PET + CT model demonstrated superior predictive power for both genes, with AUCs of 0.8146 and 0.8102 for MMR, and 0.8833 and 0.8150 for TP53 in training and test sets, respectively. MMR-related protein heterogeneity and TP53 expression differences were predominantly seen in PET images.

CONCLUSION: An efficient deep learning algorithm for endometrial cancer segmentation has been established, highlighting the enhanced predictive power of integrated PET and CT radiomics for MMR and TP53 expression. The study underscores the distinct influences of MMR and TP53 gene expression on tumor characteristics.

PMID:40474131 | DOI:10.1186/s12885-025-14392-6

BMC Med Imaging. 2025 Jun 5;25(1):204. doi: 10.1186/s12880-025-01747-5.

ABSTRACT

BACKGROUND: Previous studies have highlighted the prominent role of age in lung cancer risk, with signs of lung aging visible in computed tomography (CT) imaging. This study aims to characterize lung aging using quantitative radiomic features extracted from five delineated lung lobes and explore how age contributes to lung cancer development through these features.

METHODS: We analyzed baseline CT scans from the Wenling lung cancer screening cohort, consisting of 29,810 participants. Deep learning-based segmentation method was used to delineate lung lobes. A total of 1,470 features were extracted from each lobe. The minimum redundancy maximum relevance algorithm was applied to identify the top 10 age-related radiomic features among 13,137 never smokers. Multiple regression analyses were used to adjust for confounders in the association of age, lung lobar radiomic features, and lung cancer. Linear, Cox proportional hazards, and parametric accelerated failure time models were applied as appropriate. Mediation analyses were conducted to evaluate whether lobar radiomic features mediate the relationship between age and lung cancer risk.

RESULTS: Age was significantly associated with an increased lung cancer risk, particularly among current smokers (hazard ratio = 1.07, P = 2.81 × 10- 13). Age-related radiomic features exhibited distinct effects across lung lobes. Specifically, the first order mean (mean attenuation value) filtered by wavelet in the right upper lobe increased with age (β = 0.019, P = 2.41 × 10- 276), whereas it decreased in the right lower lobe (β = -0.028, P = 7.83 × 10- 277). Three features, namely wavelet_HL_firstorder_Mean of the right upper lobe, wavelet_LH_firstorder_Mean of the right lower lobe, and original_shape_MinorAxisLength of the left upper lobe, were independently associated with lung cancer risk at Bonferroni-adjusted P value. Mediation analyses revealed that density and shape features partially mediated the relationship between age and lung cancer risk while a suppression effect was observed in the wavelet first order mean of right upper lobe.

CONCLUSIONS: The study reveals lobe-specific heterogeneity in lung aging patterns through radiomics and their associations with lung cancer risk. These findings may contribute to identify new approaches for early intervention in lung cancer related to aging.

CLINICAL TRIAL NUMBER: Not applicable.

PMID:40474072 | DOI:10.1186/s12880-025-01747-5

Interdiscip Sci. 2025 Jun 5. doi: 10.1007/s12539-025-00721-7. Online ahead of print.

NO ABSTRACT

PMID:40474036 | DOI:10.1007/s12539-025-00721-7

Nat Cardiovasc Res. 2025 Jun 5. doi: 10.1038/s44161-025-00656-8. Online ahead of print.

ABSTRACT

Although genetic variant effects often interact nonadditively, strategies to uncover epistasis remain in their infancy. Here we develop low-signal signed iterative random forests to elucidate the complex genetic architecture of cardiac hypertrophy, using deep learning-derived left ventricular mass estimates from 29,661 UK Biobank cardiac magnetic resonance images. We report epistatic variants near CCDC141, IGF1R, TTN and TNKS, identifying loci deemed insignificant in genome-wide association studies. Functional genomic and integrative enrichment analyses reveal that genes mapped from these loci share biological process gene ontologies and myogenic regulatory factors. Transcriptomic network analyses using 313 human hearts demonstrate strong co-expression correlations among these genes in healthy hearts, with significantly reduced connectivity in failing hearts. To assess causality, RNA silencing in human induced pluripotent stem cell-derived cardiomyocytes, combined with novel microfluidic single-cell morphology analysis, confirms that cardiomyocyte hypertrophy is nonadditively modifiable by interactions between CCDC141, TTN and IGF1R. Our results expand the scope of cardiac genetic regulation to epistasis.

PMID:40473955 | DOI:10.1038/s44161-025-00656-8

J Relig Health. 2025 Jun 5. doi: 10.1007/s10943-025-02347-x. Online ahead of print.

ABSTRACT

Integrating artificial intelligence (AI) in religious education is an emerging area of research. This study explores the potential of AI and voice-activated technologies in capturing the emotional depth of chanting during spiritual practices. The study used pre-trained voice recognition models combined with deep learning to analyze vocal characteristics. The objective of the research was to develop AI algorithms for analyzing vocal characteristics and assessing the emotional states of practitioners. For this purpose, 110 first- and second-year Chinese university students majoring in vocal performance were involved. The students were divided into experimental (trained with the help of AI) and control groups (trained traditionally). The study used the correlation analysis method. The Spielberger State-Anxiety Inventory, the Positive and Negative Affect Schedule (PANAS), and the Perceived Stress Scale (PSS) were used to measure emotional states. Participants trained with AI-assisted tools demonstrated significant improvement in their voices' intonation, volume, timbre, and frequency spectrum, as well as increased calmness. Compared to the control group that did not use AI technologies, these improvements were statistically significant. Correlation analysis confirmed a strong relationship between vocal parameters and participants' emotional states. This research highlights the effectiveness of AI in religious education and opens new avenues for enhancing educational processes by providing participants with objective feedback on their spiritual practices.

PMID:40473902 | DOI:10.1007/s10943-025-02347-x

Eur Respir J. 2025 Jun 5:2401667. doi: 10.1183/13993003.01667-2024. Online ahead of print.

ABSTRACT

The formation of myofibroblast foci constitutes a hallmark pathological feature of idiopathic pulmonary fibrosis (IPF), yet the mechanism remains elusive. RNA binding motif single-stranded interacting protein 1 (RBMS1), is known to be essential for proliferation and cell cycle progression; however, its role in pulmonary fibrosis remains to be clarified.This study aimed to systematically elucidate the role and underlying mechanism of RBMS1 in pulmonary fibrosis utilising mouse primary lung fibroblasts (mPLFs), fibroblast-specific Rbms1 deletion and overexpression mice models, and lung samples from IPF patients.RBMS1 was highly expressed in both IPF patient lungs and murine bleomycin (BLM)-induced fibrotic lesions. Notably, elevated RBMS1 expression was observed in the cytoplasm of mPLFs following TGF-β1 stimulation. Rbms1 promoted lung fibroblast activation, while knockdown of Rbms1 mitigated TGF-β1-induced fibrogenesis. In vivo, overexpression impaired lung function and exacerbated pulmonary fibrosis, whereas fibroblast-specific Rbms1 deletion exhibited a significant reduction in fibrosis post-BLM treatment. Mechanistically, Rbms1 binds to Sumo2 3'UTR, enhancing the mRNA stability. Furthermore, Rbms1 induced the SUMOylation of Smad4, with lysine 158 identified as a critical SUMOylation site. Meanwhile, Sumo2 knockdown alleviated the Rbms1-driven exacerbation of pulmonary fibrosis. Importantly, the nortriptyline pharmacologically inhibited RBMS1 to ameliorate pulmonary fibrosis in mice.Collectively, our study sheds light on the regulatory role of RBMS1 in pulmonary fibrosis, highlighting its therapeutic potential for targeted antifibrotic strategies.

PMID:40473311 | DOI:10.1183/13993003.01667-2024

Eur Respir J. 2025 Jun 5;65(6):2500036. doi: 10.1183/13993003.00036-2025. Print 2025 Jun.

NO ABSTRACT

PMID:40473306 | DOI:10.1183/13993003.00036-2025

Eur Respir J. 2025 Jun 5;65(6):2500938. doi: 10.1183/13993003.00938-2025. Print 2025 Jun.

NO ABSTRACT

PMID:40473296 | DOI:10.1183/13993003.00938-2025

Nat Cardiovasc Res. 2025 Jun 5. doi: 10.1038/s44161-025-00656-8. Online ahead of print.

ABSTRACT

Although genetic variant effects often interact nonadditively, strategies to uncover epistasis remain in their infancy. Here we develop low-signal signed iterative random forests to elucidate the complex genetic architecture of cardiac hypertrophy, using deep learning-derived left ventricular mass estimates from 29,661 UK Biobank cardiac magnetic resonance images. We report epistatic variants near CCDC141, IGF1R, TTN and TNKS, identifying loci deemed insignificant in genome-wide association studies. Functional genomic and integrative enrichment analyses reveal that genes mapped from these loci share biological process gene ontologies and myogenic regulatory factors. Transcriptomic network analyses using 313 human hearts demonstrate strong co-expression correlations among these genes in healthy hearts, with significantly reduced connectivity in failing hearts. To assess causality, RNA silencing in human induced pluripotent stem cell-derived cardiomyocytes, combined with novel microfluidic single-cell morphology analysis, confirms that cardiomyocyte hypertrophy is nonadditively modifiable by interactions between CCDC141, TTN and IGF1R. Our results expand the scope of cardiac genetic regulation to epistasis.

PMID:40473955 | DOI:10.1038/s44161-025-00656-8

Mol Syst Biol. 2025 Jun 5. doi: 10.1038/s44320-025-00124-2. Online ahead of print.

ABSTRACT

In response to infection or vaccination, lymph nodes must select antigen-reactive B-cells while eliminating auto-reactive B-cells. B-cells are instructed via B-cell receptor (BCR), which binds antigen, and CD40 receptor by antigen-recognizing T-cells. How BCR and CD40 signaling are integrated quantitatively to jointly determine B-cell fate decisions remains unclear. Here, we developed a differential-equations-based model of BCR and CD40 signaling networks activating NFκB. The model recapitulates NFκB dynamics upon BCR and CD40 stimulation, and when linked to established cell decision models of cell cycle and survival control, the resulting cell population dynamics. However, upon costimulation, NFκB dynamics were correctly predicted but the predicted potentiated population expansion was not observed experimentally. We found that this discrepancy was due to BCR-induced caspase activity that may trigger apoptosis in founder cells, unless timely NFκB-induced survival gene expression protects them. Iterative model predictions and sequential co-stimulation experiments revealed how complex non-monotonic integration of BCR and CD40 signals controls positive and negative selection of B-cells. Our work suggests a temporal proof-reading mechanism for regulating the stringency of B-cell selection during antibody responses.

PMID:40473841 | DOI:10.1038/s44320-025-00124-2

NPJ Sci Food. 2025 Jun 5;9(1):95. doi: 10.1038/s41538-025-00462-3.

ABSTRACT

Determining the geographic origin of palm oil in West Africa is vital for economic, environmental, and health reasons. It enhances traceability, protects local farmers, supports conservation by monitoring deforestation, and reduces food fraud, ensuring quality and regulatory compliance. Portable Raman spectroscopy offers a rapid method to identify the origin of palm oils from West Africa. Using principal component analysis (PCA), distinct clusters in scores plots were observed which reflected the geographic origin of the palm oils, with loadings from the first principal component (PC-1) highlighting β-carotene as a major source of variation among the samples. To quantify β-carotene content, a partial least squares regression (PLS-R) model was developed in coconut oil as the base oil as it is known to be β-carotene free. Once calibrated, PLS-R was used to rank the palm oil from West Africa based on their β-carotene levels. The resulting models in coconut oil demonstrated strong linearity and predictive performance, with R² and Q² values of 0.9848 and 0.9552, respectively, alongside low root mean square errors of cross-validation (0.1282 mM) and prediction (0.0747 mM); moreover, this model allows the palm oils to be ranked based on β-carotene content which was entirely reflective of the oils position in PC-1 from PCA. These findings underscore the potential of Raman spectroscopy as an effective tool for authenticating the geographic origin of palm oil from West Africa.

PMID:40473674 | DOI:10.1038/s41538-025-00462-3

Nat Commun. 2025 Jun 5;16(1):5248. doi: 10.1038/s41467-025-60535-5.

ABSTRACT

SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complexes displace nucleosomes to promote the access of transcription factors to enhancers and promoters. Despite the critical roles of SWI/SNF in animal development and tumorigenesis, how signaling pathways recruit SWI/SNF complexes to their target genes is unclear. Here, we demonstrate that target gene activation mediated by β-catenin, the essential transcriptional coactivator in the Wnt signal transduction pathway, requires ubiquitylation of the SWI/SNF component Brahma-related gene-1 (BRG1) by the E3 ubiquitin ligase Thyroid Hormone Receptor Interactor 12 (TRIP12). TRIP12 depletion in Drosophila, zebrafish, mouse organoids, and human cells attenuates Wnt signaling. Genetic epistasis experiments place TRIP12 activity downstream of the β-catenin destruction complex. TRIP12 interacts with and ubiquitylates BRG1, and BRG1 depletion blocks TRIP12-mediated Wnt pathway activation. TRIP12 promotes BRG1 binding to β-catenin in the presence of Wnt. Our findings support a model in which TRIP12 ubiquitylates BRG1 in the presence of Wnt and promotes its interaction with β-catenin in the nucleus, in order to recruit SWI/SNF to Wnt target genes. Our studies suggest a general mechanism by which cell signaling induces the interaction between BRG1 and pathway-specific transcription factors to recruit SWI/SNF complexes to their appropriate target genes.

PMID:40473626 | DOI:10.1038/s41467-025-60535-5

Eur Respir J. 2025 Jun 5:2401667. doi: 10.1183/13993003.01667-2024. Online ahead of print.

ABSTRACT

The formation of myofibroblast foci constitutes a hallmark pathological feature of idiopathic pulmonary fibrosis (IPF), yet the mechanism remains elusive. RNA binding motif single-stranded interacting protein 1 (RBMS1), is known to be essential for proliferation and cell cycle progression; however, its role in pulmonary fibrosis remains to be clarified.This study aimed to systematically elucidate the role and underlying mechanism of RBMS1 in pulmonary fibrosis utilising mouse primary lung fibroblasts (mPLFs), fibroblast-specific Rbms1 deletion and overexpression mice models, and lung samples from IPF patients.RBMS1 was highly expressed in both IPF patient lungs and murine bleomycin (BLM)-induced fibrotic lesions. Notably, elevated RBMS1 expression was observed in the cytoplasm of mPLFs following TGF-β1 stimulation. Rbms1 promoted lung fibroblast activation, while knockdown of Rbms1 mitigated TGF-β1-induced fibrogenesis. In vivo, overexpression impaired lung function and exacerbated pulmonary fibrosis, whereas fibroblast-specific Rbms1 deletion exhibited a significant reduction in fibrosis post-BLM treatment. Mechanistically, Rbms1 binds to Sumo2 3'UTR, enhancing the mRNA stability. Furthermore, Rbms1 induced the SUMOylation of Smad4, with lysine 158 identified as a critical SUMOylation site. Meanwhile, Sumo2 knockdown alleviated the Rbms1-driven exacerbation of pulmonary fibrosis. Importantly, the nortriptyline pharmacologically inhibited RBMS1 to ameliorate pulmonary fibrosis in mice.Collectively, our study sheds light on the regulatory role of RBMS1 in pulmonary fibrosis, highlighting its therapeutic potential for targeted antifibrotic strategies.

PMID:40473311 | DOI:10.1183/13993003.01667-2024

Plant Physiol. 2025 Jun 6:kiaf232. doi: 10.1093/plphys/kiaf232. Online ahead of print.

NO ABSTRACT

PMID:40473241 | DOI:10.1093/plphys/kiaf232

Protein Expr Purif. 2025 Jun 3:106752. doi: 10.1016/j.pep.2025.106752. Online ahead of print.

ABSTRACT

The yeast cadmium factor 1 protein (Ycf1p) is an ATP-binding cassette (ABC) transporter located in the vacuolar membrane and is responsible for transporting glutathione-conjugated metals from the cytoplasm into the vacuole. Ycf1p contains the ABC core structure of two transmembrane domains (TMD1, TMD2) and two nucleotide-binding domains (NBD1, NBD2). As a member of the C-subfamily of ABC proteins (ABCC), Ycf1p also contains an N-terminal extension comprised of an additional TMD (TMD0) and L0 linker. Although high-resolution structures of many ABC transporters have been determined, the NBDs can be at low resolution in cryo-EM maps and thus, studies of the isolated cytosolic NBDs are crucial for obtaining molecular-level details of the dynamics of these catalytic entities, for example. In this study, we present a scheme for obtaining samples of NBD2 from the yeast cadmium factor protein 1 (Ycf1p) in a soluble, monomeric, and functional form. While production of NBD1 from Ycf1p and other ABC proteins has been accomplished, generating samples of NBD2 from different ABC proteins has been elusive for the most part, particularly for ABCC proteins. We show that NBD2 preparation necessitates minimizing dimerization and aggregation of the protein at multiple steps during the purification, which is accomplished by employing a solubility tag, eliminating nucleotides from the buffers, and limiting the duration of spin concentrating steps. This work lays the foundation for detailed studies of Ycf1p NBD2 and provides an outline for optimizing the generation of NBD2 from other ABC proteins.

PMID:40473008 | DOI:10.1016/j.pep.2025.106752

Bioorg Med Chem Lett. 2025 Jun 3:130293. doi: 10.1016/j.bmcl.2025.130293. Online ahead of print.

ABSTRACT

The papain-like protease (PLpro) of SARS-CoV-2 has been identified as a pivotal enzyme in viral replication, indicating it a promising target for drug discovery. Utilizing a virtual screening strategy, compound 1 with the N-(3-(5-amino-1H-pyrazol-3-yl)phenyl) benzenesulfonamide scaffold was discovered as a hit targeting PLpro. Structural modification from virtually screened hit 1 led to the development of a series of substituted 3-phenyl-1H-5-pyrazolylamide derivatives. Notably, compounds 14 h and 14e exhibited improved PLpro inhibitory activity (IC50 = 14.2 μM and 12.0 μM, respectively) and low cytotoxicity. Further biological evaluation revealed that compound 14e with a thiophene aldehyde group displayed potent binding activity (KD = 1.86 μM). This 3-phenyl-1H-5-pyrazolylamide scaffold offers significant potential for further development as a novel class of PLpro inhibitors.

PMID:40473007 | DOI:10.1016/j.bmcl.2025.130293

Cell Syst. 2025 Jun 2:101300. doi: 10.1016/j.cels.2025.101300. Online ahead of print.

ABSTRACT

Systems biology offers a view of the cell as an input-output device: a biochemical network (or cellular "processor") that interprets cues from the microenvironment to drive cell fate. Advancements in single-cell technologies are unlocking the cellular black box, revealing heterogeneity in seemingly homogeneous cell populations. But are these differences technical variability or biology? In this review, we explore this question through a systems biology lens, offering a framework for conceptualizing heterogeneity from the cell's perspective and summarizing systems and synthetic biology tools for capturing heterogeneity. While cellular inputs shape the probability of attaining particular fates, each cell spins a stochastic "wheel of fate." Applying this framework, we explore heterogeneity in two case studies: human pluripotent stem cell (hPSC) culture and beta cell differentiation. Looking forward, we discuss how a systems approach to heterogeneity may enable more predictable outcomes in stem cell research, with broad implications for developmental biology and regenerative medicine.

PMID:40472847 | DOI:10.1016/j.cels.2025.101300

IET Syst Biol. 2025 Jan-Dec;19(1):e70015. doi: 10.1049/syb2.70015.

ABSTRACT

ADAMTS5, a member of the ADAMTS family, exhibits crucial biological roles, including protein shedding, proteolysis, and cell migration. Its relevance in breast cancer (BC) was explored through an integrative approach combining high-throughput analyses, database validations, and experimental confirmation. ADAMTS5 expression was significantly reduced in BC samples, as verified by microarray analysis, qRT-PCR, and public database resources. A protein-protein interaction network revealed five proteins-COL10A1, COL11A1, COMP, MMP1 and SDC1-that interact with ADAMTS5 and are primarily associated with the ECM-receptor interaction pathway. These proteins also engage in cell cycle checkpoint signalling, emphasising their potential role in tumour progression. Survival analysis of BC samples identified a novel prognostic signature based on ADAMTS5-related proteins. The study extended to coding and noncoding RNA interactions, identifying lncRNAs as key regulators. CRNDE acts as a ceRNA for ADAMTS5, modulating its expression via hsa-miR-135b-3p. Meanwhile, BAIAP2-AS1 interacts directly with ADAMTS5, offering another layer of regulatory control and prognostic value. These findings position ADAMTS5 as a vital player in BC biology, with its low expression linked to critical pathways and survival outcomes. The identified lncRNA-mediated regulatory mechanisms add depth to understanding ADAMTS5's role and suggest potential targets for therapeutic development. This study underscores ADAMTS5's potential as a biomarker and its broader implications in unravelling BC molecular mechanisms.

PMID:40472834 | DOI:10.1049/syb2.70015

J Environ Manage. 2025 Jun 4;389:126075. doi: 10.1016/j.jenvman.2025.126075. Online ahead of print.

ABSTRACT

The spread of aquatic invasive species (AIS) presents a pressing challenge for global biodiversity, with freshwater ecosystems being particularly affected. The connection of watersheds throughout Europe by the construction of artificial shipping canals has created novel invasion pathways, but may also provide critical infrastructure to counter range expansion by implementation of different barrier solutions. Here, we critically review the efficacy, applicability and limitations of dispersal barriers against AIS in shipping canals considering fishes, invertebrates, algae, bacteria and fungi. Despite the wide spread of AIS and their known detrimental effects on aquatic ecosystems, research focusing on barriers for AIS in shipping canals is rather limited and predominantly concentrated on a few species of fish. Out of 180 screened studies, only 32 examined the efficacy of technologies such as electric fields, acoustic signals, strobe light, air-bubble curtains, CO2 and pheromones as non-physical barriers. Efficacy and applicability was mostly tested in laboratory setups and strongly species-dependent, requiring a site-specific identification of the most useful barrier technology. Major limitations to barrier implementation include undesired and unknown side effects on non-target species, humans and the environment. To preserve the ecological integrity of freshwater ecosystems across transboundary and inland watersheds, future research should tackle these challenges by increasing the number of studies under realistic field conditions to allow evidence-based decision making on the management of AIS.

PMID:40472533 | DOI:10.1016/j.jenvman.2025.126075

Comput Biol Med. 2025 Jun 3;194:110456. doi: 10.1016/j.compbiomed.2025.110456. Online ahead of print.

ABSTRACT

BACKGROUND AND OBJECTIVE: Coronary heart disease (CHD) is a leading cause of morbidity and mortality globally, frequently accompanied by major depressive disorder (MDD), which exacerbates clinical outcomes. While Guanxinning (GXN) has demonstrated efficacy in improving cardiac function and reducing angina symptoms in CHD patients, its potential role in alleviating MDD symptoms has not been extensively studied. This study aims to explore the potential therapeutic effects of GXN on CHD and MDD through the regulation of S1PR3.

METHODS: We utilized bioinformatics, network pharmacology, and Mendelian randomization to identify S1PR3 as a key therapeutic target for CHD and MDD. Molecular docking simulations were conducted to validate the binding affinity between GXN components and S1PR3.

RESULTS: Our findings indicate that CHD is a risk factor for MDD, and the downregulation of S1PR3 expression in CHD patients is associated with the onset of MDD. Molecular docking analysis demonstrated that GXN can effectively bind to S1PR3, suggesting that GXN may modulate S1PR3 expression levels to prevent MDD in CHD patients.

CONCLUSION: This study identifies S1PR3 as a critical therapeutic target for the comorbidity of CHD and MDD. GXN has the potential to treat CHD and MDD by regulating S1PR3 expression levels. Although further validation through animal and cell-based experiments is needed, our findings provide a foundational understanding of the molecular mechanisms and highlight the therapeutic potential of GXN in dual heart therapy.

PMID:40472508 | DOI:10.1016/j.compbiomed.2025.110456