{"title":"Longitudinal <sup>1</sup>H NMR metabolomics of serum in a chronic temporal lobe epilepsy model reveals systemic metabolic remodeling.","authors":"Veronica Ghini, Lucrezia Cosottini, Miriana Scordino, Nicolò Ricciardi, Giulia Urone, Giuditta Gambino, Valentina Di Liberto, Paola Turano","doi":"10.3389/fmolb.2026.1882162","DOIUrl":"10.3389/fmolb.2026.1882162","url":null,"abstract":"<p><strong>Introduction: </strong>Temporal lobe epilepsy is associated with systemic metabolic alterations that may evolve during disease progression and in response to pharmacological treatment. This study employed a longitudinal <sup>1</sup>H NMR-based metabolomics approach to characterize the serum metabolic profile of a chronic pilocarpine-induced rat model of temporal lobe epilepsy.</p><p><strong>Methods: </strong>Serum samples were collected longitudinally to identify phase-specific metabolic signatures. Following phenobarbital administration, animals were classified as drug-sensitive or drug-resistant according to their treatment response. The resulting metabolic profiles were investigated using multivariate and univariate statistical analyses.</p><p><strong>Results: </strong>The analysis revealed progressive systemic metabolic remodeling characterized by extensive alterations in lipid-related signals and significant increases in the ketone bodies 3-hydroxybutyrate and acetoacetate, as well as in glutamine. Following phenobarbital treatment, OPLS-DA showed a strong metabolic similarity between the drug-sensitive and drug-resistant groups, which occupied nearly identical metabolic spaces. Nevertheless, after stratification, creatine emerged as the only significantly different metabolite between responders and non-responders (p = 0.001).</p><p><strong>Discussion: </strong>The convergence of the metabolic profiles of drug-sensitive and drug-resistant animals suggests that the systemic effects of chronic epilepsy and phenobarbital treatment dominate the serum metabolome, potentially masking subtle molecular signatures associated with drug resistance. Creatine represents a notable exception and warrants further investigation as a potential marker distinguishing responders from non-responders.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1882162"},"PeriodicalIF":4.4,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13572219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Feng Huang, Jung-Yin Fong, Chin Tat Ng, Karthikkumar Venkatachalam, Mohammed Abdullah Alshawsh, Chun-Wai Mai, Yik-Ling Chew, Muralidharan Anbalagan, Ravishankar Ram Mani, Malarvili Selvaraja
{"title":"Crucial role of telomere maintenance-related genes in survival prediction and subtype identification in colorectal cancer.","authors":"Feng Huang, Jung-Yin Fong, Chin Tat Ng, Karthikkumar Venkatachalam, Mohammed Abdullah Alshawsh, Chun-Wai Mai, Yik-Ling Chew, Muralidharan Anbalagan, Ravishankar Ram Mani, Malarvili Selvaraja","doi":"10.3389/fmolb.2026.1728178","DOIUrl":"10.3389/fmolb.2026.1728178","url":null,"abstract":"<p><strong>Background: </strong>Telomere maintenance-related genes (TMRGs) are implicated in Colorectal cancer (CRC) development, but their prognostic value and clinical relevance remain insufficiently explored. This study aims to develop a TMRG-based prognostic model and elucidate its clinical utility in CRC management.</p><p><strong>Methods: </strong>The Cancer Genome Atlas database was utilized to download RNA-seq data from 638 CRC and 51 control samples. Differential expressed genes were screened and intersected with 2086 TMRGs, resulting in the identification of 976 TMRGs. Through univariate and multivariate Cox regression analysis, a prognostic model comprising three telomere maintenance-related biomarkers (<i>PDE1B, TFAP2B, and HSPA1A</i>) was developed and validated using an external dataset. By integrating the model risk score with clinical features, a nomogram was constructed to predict the survival outcomes of CRC patients. Additionally, an in-depth investigation of the immuno-infiltration, functional variation and drug sensitivity analysis were performed in two risk subgroups defined by the prognostic model. Finally, the functional significance of <i>PDE1B</i> in CRC cell lines was investigated through MTT assays, cell colony formation assays, transwell assays and flow cytometry.</p><p><strong>Results: </strong>A total of 976 DE-TMRGs were enriched in telomere/DNA replication pathways. A three-gene signature (PDE1B, TFAP2B, and HSPA1A) stratified patients into high- and low-risk groups with divergent survival (AUC >0.60, validated externally). High-risk patients had advanced N/M stages, elevated M0/M2 macrophages, reduced CD4<sup>+</sup> memory T cells, and upregulated immune checkpoints. Nomogram integrating risk score, age, and N/M stage accurately predicted 1-/3-/5-year survival. Low-risk patients showed greater 5-fluorouracil sensitivity. <i>PDE1B</i> expression was significantly reduced in CRC tissues and correlated with advanced stages. Functional assays confirmed PDE1B overexpression suppressed proliferation, migration, invasion, and induced apoptosis in CRC cells.</p><p><strong>Conclusion: </strong>This study identifies a moderately predictive telomere maintenance-related gene signature as an independent prognostic predictor in CRC. The risk stratification model effectively discriminates patients with distinct survival patterns, tumor microenvironments, and therapeutic responses, while the integrated nomogram offers additional reference information for survival analysis, albeit with only moderate predictive accuracy. These findings indicate telomere maintenance-related gene signature could serve as a preliminary auxiliary risk stratification tool for postoperative CRC patients, <i>PDE1B</i> may also serve as a potential epithelial tumor-suppressor target for future preclinical studies.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1728178"},"PeriodicalIF":4.4,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13561823/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148955185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sara Afzali Jaktajdinani, Lili Hegedűs, Nargis Karatayeva, Roberta Fajka-Boja, Peter Burkovics
{"title":"The function of Mgs1/WRNIP1 in genome maintenance.","authors":"Sara Afzali Jaktajdinani, Lili Hegedűs, Nargis Karatayeva, Roberta Fajka-Boja, Peter Burkovics","doi":"10.3389/fmolb.2026.1923317","DOIUrl":"10.3389/fmolb.2026.1923317","url":null,"abstract":"<p><p>Preservation of genomic integrity during replication is challenging, because replication forks are often stalled by several forms of DNA damage or stable secondary DNA structures. Prolonged stalling of the replication fork can lead to incomplete replication, which may induce double strand breaks, genome rearrangements and cell death. Therefore, several DNA repair mechanisms evolved to rescue stalled replication forks, which can elaborate in error-free or error-prone manners. The pathway selection and the fine tuning of the collaboration between different DNA repair proteins involved in the rescue of the stalled replication fork are very important. Based on our recent knowledge, yeast Mgs1 and its human homologue WRNIP1 proteins can be excellent candidates for this fine-tuning regulator function. In this review we summarize our current knowledge about them and try to point out the most important future steps to prove this hypothesis.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1923317"},"PeriodicalIF":4.4,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiu-Juan Xu, Min Wang, Xiao-Ping Li, Wei-Chen Zhang, Shi-Tong Zeng, Qing-Zhao Shi, Yi-Wei Ma, Bin-Bin Lu, Shan Liu, Ding-Zhong Wang, Ren-Qi Wang, Jun Hu
{"title":"Geographic authentication of premium tobacco extracts using machine learning models trained on LC-HRMS fingerprints.","authors":"Xiu-Juan Xu, Min Wang, Xiao-Ping Li, Wei-Chen Zhang, Shi-Tong Zeng, Qing-Zhao Shi, Yi-Wei Ma, Bin-Bin Lu, Shan Liu, Ding-Zhong Wang, Ren-Qi Wang, Jun Hu","doi":"10.3389/fmolb.2026.1898152","DOIUrl":"10.3389/fmolb.2026.1898152","url":null,"abstract":"<p><strong>Introduction: </strong>The geographic origin of premium tobacco extracts fundamentally shapes their sensory profiles and commercial value, but authenticating these complex matrices remains a formidable analytical challenge. Conventional nontargeted analysis workflows typically rely on a minute fraction of structurally annotated metabolites, thereby discarding the vast majority of unannotated yet highly specific chemical markers. To address this limitation, this study introduces a geographic authentication framework utilizing machine learning models trained on characteristic ion feature (CIF) fingerprints.</p><p><strong>Methods: </strong>A large-scale dataset of 1,697 tobacco samples was analyzed using liquid chromatography-high resolution mass spectrometry coupled with a data-independent acquisition strategy. Rigorous statistical filtering was applied to isolate CIFs and strip away the shared background metabolome. To evaluate the samples, univariate thresholding based on pattern similarity (dot product) and marker intensity ratios (R score) was initially tested. To overcome the vulnerability of univariate methods to batch effects and overlapping chemical profiles, optimized multivariate machine learning models were also deployed. The models were evaluated under a strict Leave-One-Batch-Out cross-validation framework to ensure robust cross-batch generalization.</p><p><strong>Results: </strong>Statistical filtering effectively stripped away over 90% of the shared background metabolome, isolating 47,543 CIFs for Zimbabwe tobacco and 3,646 CIFs for Yunnan tobacco. Univariate thresholding achieved a maximum balanced accuracy of 77.9% but proved too rigid. Under cross-validation, the multivariate Random Forest (RF) classifier demonstrated strong predictive performance, achieving a balanced accuracy of 74.6% for Zimbabwe tobacco and successfully detecting economically motivated adulteration across a wide dilution range (0-1,000 ppm). Conversely, both univariate and multivariate methods failed to achieve robust authentication for the Yunnan extracts. This underperformance was driven by severe intra-group heterogeneity stemming from diverse suppliers and heterogeneous processing treatments, which heavily diluted universal characteristic features.</p><p><strong>Discussion: </strong>Ultimately, this hybrid strategy provides a scalable tool for the industrial verification of consistent premium extracts. Furthermore, the challenges encountered with the Yunnan samples underscore the necessity of cohort-specific modeling when dealing with highly diverse agricultural products that are subjected to varied processing treatments.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1898152"},"PeriodicalIF":4.4,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Itraconazole induced ferroptosis in acute myeloid leukemia cells through TP53INP1.","authors":"Yan Qi, Changhao Han, Yizhang Lin, Shidi Cheng, Yuanting She, Meijuan Zhang, Huan Xie, Guangming Yang, Dongfeng Zeng","doi":"10.3389/fmolb.2026.1890539","DOIUrl":"10.3389/fmolb.2026.1890539","url":null,"abstract":"<p><strong>Background: </strong>Itraconazole (ITRA) is a broad-spectrum antifungal agent approved by the Food and Drug Administration (FDA). It has been shown to inhibit cancer growth, but the underlying molecular mechanism of itraconazole-induced cell death in acute myeloid leukemia (AML) remains largely elusive.</p><p><strong>Methods: </strong>CCK-8 assay, colony-formation assay, flow cytometry, Western blotting, reactive oxygen species (ROS) detection, and ferroptosis analysis were performed to reveal the role and underlying mechanisms of itraconazole in AML cell lines. Itraconazole has also done research on <i>in vivo</i> experiments.</p><p><strong>Results: </strong>Itraconazole significantly inhibits the viability of AML cell lines and arrests the cell cycle at the G2/M phase. Further investigations reveal that itraconazole effectively induces ferroptosis in AML cells, as evidenced by iron dependency and mitochondrial dysfunction. Notably, the TP53INP1 signaling pathway is markedly upregulated in itraconazole-treated AML cells. Knockdown of TP53INP1 significantly attenuates itraconazole-induced ferroptosis by regulating iron metabolism, which in turn restores mitochondrial function and elevates SLC7A11 and GPX4 levels. Meanwhile, <i>in vivo</i> experiments demonstrate that itraconazole impairs AML progression. It is worth noting that concomitant changes in apoptotic markers were also observed, suggesting that itraconazole may simultaneously trigger both apoptotic and ferroptotic pathways, which may coexist in AML cells.</p><p><strong>Conclusion: </strong>Our findings suggest that itraconazole exerts anti-leukemic effects associated with ferroptosis induction involving TP53INP1, though apoptosis may coexist, supporting its further evaluation as a therapeutic candidate for AML.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1890539"},"PeriodicalIF":4.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Katarzyna Miniewska, Patrycja Mojsak, Sandra Chmielewska, Paulina Choinska, Joanna Godzien, Lukasz Labieniec, Andrzej Andrejczuk, Jarna Hannukainen, Vesa Oikonen, Kirsi Virtanen, Pirjo Nuutila, Michal Ciborowski, Katarzyna Maliszewska, Adam J Kretowski
{"title":"Activation of human brown adipocytes alters the plasma fatty acid profile.","authors":"Katarzyna Miniewska, Patrycja Mojsak, Sandra Chmielewska, Paulina Choinska, Joanna Godzien, Lukasz Labieniec, Andrzej Andrejczuk, Jarna Hannukainen, Vesa Oikonen, Kirsi Virtanen, Pirjo Nuutila, Michal Ciborowski, Katarzyna Maliszewska, Adam J Kretowski","doi":"10.3389/fmolb.2026.1842960","DOIUrl":"10.3389/fmolb.2026.1842960","url":null,"abstract":"<p><strong>Introduction: </strong>Even though brown adipose tissue (BAT) has recently been identified as a possible target for combating obesity and type 2 diabetes, neither the mechanisms of its activation nor its relationships to clinical parameters are clearly defined. Metabolomics enables the simultaneous analysis of multiple classes of compounds, thus seems to be a perfect tool to study this topic. This study aimed to explore alterations during cold exposure (CE) associated with the activation of BAT.</p><p><strong>Materials and methods: </strong>Twenty-five healthy male adults underwent 2 hours of CE followed by PET-MRI. Afterwards, they were divided into two groups, depending on BAT presence (BATpos or BATneg). The levels of metabolites were measured in plasma samples at three time points: before, after one, and 2 hours of CE, using a standard gas chromatography-mass spectrometry (GC-MS) method for metabolite profiling.</p><p><strong>Results: </strong>In the BATpos group, the levels of linoleic, oleic, and palmitic acids were significantly increased after 120 min of CE compared to the baseline. These changes were absent in the BATneg group. When comparing the BATpos and BATneg groups, we observed that the BATpos group had significantly lower baseline level of succinic acid. After 60 min of CE, the BATpos group showed significantly increased levels of linoleic, oleic and trans-13-octadecenoic acid. The differences in oleic acid persisted for another hour.</p><p><strong>Conclusion: </strong>Between-group differences in the level of fatty acids during CE, along with the BATpos group-specific alterations during CE, suggest that the activation of BAT affects lipid metabolism.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1842960"},"PeriodicalIF":4.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13553035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ying Chen, Jing Xie, Li Chen, Xuezhen Peng, Guicong Ding, Guo-Bing Wang, Li Zhang
{"title":"Metabolic profiling of severe early childhood caries and black stain: pathway and biomarker discovery in 3-6-year-olds.","authors":"Ying Chen, Jing Xie, Li Chen, Xuezhen Peng, Guicong Ding, Guo-Bing Wang, Li Zhang","doi":"10.3389/fmolb.2026.1838384","DOIUrl":"10.3389/fmolb.2026.1838384","url":null,"abstract":"<p><p>The present study aims to identify the key metabolic compounds of supragingival plaque and potential metabolic pathways associated with severe early childhood caries (S-ECC) in preschool children, and to provide a basis for screening candidate biomarkers that could be beneficial to clinical practice guidelines. A cohort of 93 children, including 32 healthy controls (HC group), 31 children with S-ECC (SECC group) and 30 children with S-ECC and black stain (SECCBS group), were recruited. Supragingival plaques were collected for UHPLC-MS analyses followed by bioinformatics analysis. Differential metabolites (DMs) were screened through Partial Least Squares Discriminatory Analysis (PLS-DA) and enriched in KEGG pathways. Ecological network analysis and WGCNA were performed to construct co-expression networks. Ten machine learning (ML) models were optimized by feature selection and hyperparameter tuning, and evaluated using the area under the ROC curve (AUC), sensitivity, specificity, precision, and predictability comparison. A total of 1,069 metabolites were detected, with 497 annotated into 40 KEGG pathways, primarily amino acid and lipid metabolism. We identified 134 DMs between the HC and SECC groups, and 49 DMs between the SECC and SECCBS groups. WGCNA identified 32 co-expression modules in each paired comparison. In the HC-SECC comparison, the top correlated module pathways (neuroactive ligand-receptor interaction and pyrimidine metabolism) aligned precisely with the KEGG enrichment results of the DMs. In the SECC-SECCBS comparison, biosynthesis of unsaturated fatty acids and fatty acid degradation were uniquely enriched. For clinical prediction, the random forest (RF) model achieved the highest AUC (98.38) in the HC-SECC group, while the SVM-Poly model was superior in the SECC-SECCBS group (AUC = 95.10). The supragingival plaque metabolome is discernibly different among healthy children, those with severe caries, and those with black stain. Key metabolites including uracil, uridine 5'-diphosphate, cytosine, epinephrine, uridine, and deoxycytidylic acid are closely associated with dental caries occurrence and represent promising targets for early diagnosis. Additionally, Glycerophospho-N-palmitoyl ethanolamine (GP-NPEA) and lipid metabolic adaptations (such as unsaturated fatty acid pathways) in the SECCBS group provide a novel mechanistic explanation for the lower caries susceptibility and the pigment formation associated with black stain. These biomarkers offer valuable insights for precision risk stratification and personalized therapeutic strategies in pediatric dentistry.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1838384"},"PeriodicalIF":4.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541509/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Polina Anisimova, Anastasia Filat'eva, Victor Tarabykin, Elena Kondakova
{"title":"Nonsense-mediated mRNA decay and associated splicing patterns in neurodevelopmental disorders.","authors":"Polina Anisimova, Anastasia Filat'eva, Victor Tarabykin, Elena Kondakova","doi":"10.3389/fmolb.2026.1914793","DOIUrl":"10.3389/fmolb.2026.1914793","url":null,"abstract":"<p><p>Nonsense-mediated mRNA decay (NMD) is a basic post-transcriptional mechanism ensuring the fidelity of many biological processes including brain development. Together with alternative splicing, it regulates the inclusion of poison exons. NMD is involved in the control of multiple processes during brain development such as neural progenitor proliferation and differentiation, neuronal migration, axonal guidance, and synaptic plasticity. Under physiological conditions, this mechanism safeguards neuronal identity and the functional maturation of the brain. When disrupted, the consequences range from structural cerebral anomalies to cognitive impairment and epilepsy. This review examines NMD-mediated regulatory mechanisms across different stages of brain development. Special emphasis is placed on how dysfunction in NMD pathway components-specifically core degradation factors, the exon junction complex, and neuron-specific splicing regulators-underpins an extensive array of neurodevelopmental disorders (NDDs). Furthermore, we delineate the relationship between the position of a premature termination codon (PTC) within a transcript and the resulting molecular outcome. While the degradation of aberrant mRNAs often leads to haploinsufficiency, their escape from NMD might result in the accumulation of truncated proteins with dominant-negative effects, thereby causing specific clinical phenotypes in affected patients. Elucidating these mechanisms is essential for both the interpretation of variant pathogenicity and the development of targeted therapeutic strategies.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1914793"},"PeriodicalIF":4.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13542418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Changfu Feng, Xiaojing Liu, Subi Nijiati, Xiangbo Ma, Honglin Yang
{"title":"Retrospective analysis of micronutrient status and prostate health: linking serum zinc, selenium, and vitamin D levels to prostate-specific antigen and urinary tract function.","authors":"Changfu Feng, Xiaojing Liu, Subi Nijiati, Xiangbo Ma, Honglin Yang","doi":"10.3389/fmolb.2026.1779179","DOIUrl":"10.3389/fmolb.2026.1779179","url":null,"abstract":"<p><strong>Background: </strong>Micronutrients such as zinc, selenium, and vitamin D play a crucial role in prostate physiology. Deficiencies in these nutrients may be associated with prostate-specific antigen (PSA) levels and with impaired urinary tract parameters, including the International Prostate Symptom Score (IPSS), maximum urinary flow rate (Qmax), and post-void residual (PVR) volume. This retrospective study evaluated the association between serum micronutrient status and prostate health indicators in adult men.</p><p><strong>Methods: </strong>Medical records of 400 men aged ≥45 years who underwent prostate evaluation between 2019 and 2022 were retrospectively analyzed. Serum zinc, selenium, and 25-hydroxyvitamin D levels were recorded alongside PSA values and urinary tract parameters, including IPSS, Qmax, and PVR volume. Based on reference ranges, participants were categorized into low- or normal-micronutrient groups. Correlation analyses and multivariable logistic regression were performed to identify independent predictors of elevated PSA (>4 ng/mL) and severe urinary symptoms (IPSS ≥20).</p><p><strong>Results: </strong>120 participants exhibited low micronutrient levels. Compared with men with normal levels, this group showed significantly higher PSA (5.2 ± 2.8 vs. 2.9 ± 1.5 ng/mL), higher IPSS scores (16.5 ± 5.8 vs. 10.2 ± 5.2), lower Qmax (11.2 ± 4.1 vs. 16.1 ± 4.7 mL/s), and higher PVR (61.7 ± 20.3 vs. 42.2 ± 18.5 mL) (all p < 0.001). Serum zinc, selenium, and vitamin D levels were inversely correlated with PSA and IPSS and positively correlated with Qmax (all p < 0.001). In multivariable regression analysis, low zinc (OR 2.48; 95% CI: 1.45-4.23), low selenium (OR 2.12; 95% CI: 1.27-3.52), and low vitamin D (OR 1.87; 95% CI: 1.11-3.16) were independent predictors of elevated PSA.</p><p><strong>Conclusion: </strong>Micronutrient deficiencies were associated with altered PSA levels and impaired urinary tract function. Monitoring and correcting micronutrient deficiencies may represent a valuable component of prostate health management, though prospective studies are needed to confirm causality.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1779179"},"PeriodicalIF":4.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vaishnavi Gopalakrishnan, Amal Fahma, Rajesh Raju, Sowmya Soman
{"title":"Current insights into PHF14: molecular features and functional roles.","authors":"Vaishnavi Gopalakrishnan, Amal Fahma, Rajesh Raju, Sowmya Soman","doi":"10.3389/fmolb.2026.1858432","DOIUrl":"10.3389/fmolb.2026.1858432","url":null,"abstract":"<p><p>Plant Homeodomain Finger Protein 14 (PHF14) is a known epigenetic regulator involved in chromatin-mediated gene regulation. PHF14 belongs to the plant homeodomain (PHD) family, and possesses four PHD zinc-finger domains. The N-terminal PHD1 and PHD2 domain of PHF14 mediate histone recognition through specific PHD1-ZnK-PHD2 (PZP) cassettes and thereby contribute to the regulation of transcriptional activation and gene silencing. PHF14 plays a role in regulating essential cellular processes such as the cell cycle, mesenchymal proliferation, DNA damage response, and B-cell proliferation. Genetic variants of PHF14 have been identified across multiple clinical conditions, underscoring its physiological and pathologic relevance. Over the past 5 years, PHF14 has garnered substantial attention for its dysregulation or sequence variation associated with various cancers. PHF14-mediated interactions are implicated in neurodevelopmental disorders and also contribute to lung and renal fibrosis, as well as Dandy-Walker syndrome, underscoring its role in diverse pathological conditions. This review summarizes current knowledge on PHF14 structure, interaction partners, molecular functions, associated signaling pathways, and roles in diseases.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1858432"},"PeriodicalIF":4.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}