DNA and cell biology最新文献

{"title":"The Single-Cell Atlas Revolution: Integrating Lineage, Space, and Evolution to Decode Animal Biology.","authors":"Shahab Ur Rehman, Rahmat Ali, Hosameldeen Mohamed Husien, Mengzhi Wang","doi":"10.1177/10445498261460199","DOIUrl":"10.1177/10445498261460199","url":null,"abstract":"<p><p>The advent of single-cell RNA sequencing (scRNA-seq) has fundamentally transformed biological research, converting our understanding of cellular diversity from a purely conceptual idea into a quantifiable, applicable, and observable reality. Early efforts successfully created catalogs of cell types across diverse tissues and species, delivering an effective inventory of the components that make up complex animal systems. Yet the field now stands at a crossroads; rather than bringing clarity, the ever-growing number of cellular atlases threatens to flood and overwhelm it. In this review, we argue that the next evolution of scRNA-seq must integrate three essential pillars: temporal dynamics, spatial information, and evolutionary conservation. We have entered the era of predictive biology, moving beyond simple inventories to build dynamic, multispecies, spatially resolved comparative meta-atlases. This new approach seeks not only to understand the fundamental processes of development, physiology, and disease but also to predict cellular behaviors and their evolutionary trajectories, ultimately achieving a mechanistic understanding of life's complexity.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"431-449"},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148586385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibroblast Growth Factor 18 Regulates Mitochondrial Function to Alleviate Myocardial Ischemia-Reperfusion Injury in Rats.","authors":"Haijiao Yang, Guanglei He, Xiaojing Cui, Fei Li","doi":"10.1177/10445498261458185","DOIUrl":"10.1177/10445498261458185","url":null,"abstract":"<p><p>The purpose of this work was to examine the function of fibroblast growth factor 18 (FGF18) in rat myocardial ischemia-reperfusion injury (MIRI) and elucidate its relationship to mitochondrial function through the Sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator 1 (SIRT1/PGC-1α) pathway. To evaluate myocardial infarct size, pathological alterations, cardiomyocyte injury, mitochondrial state, oxidative stress, and SIRT1/PGC-1α protein expression, FGF18-knockdown and FGF18-overexpression rat MIRI models were created. H9c2 cardiomyocytes were used to create an <i>in vitro</i> hypoxia-reoxygenation (H/R) model, and FGF18-overexpressing H9c2 cells were given the SIRT1 inhibitor EX-527. We detected the effects of FGF18-mediated regulation of the SIRT1/PGC-1α pathway on H/R-induced alterations in H9c2 cells, including cell viability, mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential, apoptotic rate, and the protein expression of FGF18, SIRT1, PGC-1α, and mitofusin 1 (Mfn1). Furthermore, we performed a protein immunoprecipitation (IP)-protein acetylation assay to determine whether FGF18 influences the acetylation level of PGC-1α through the regulation of SIRT1. Results showed that FGF18 overexpression upregulated SIRT1/PGC-1α/Mfn1 expression, improved mitochondrial function, reduced oxidative stress, and enhanced H9c2 survival under H/R, while FGF18 knockdown had opposite effects. Moreover, FGF18 overexpression inhibited H/R-induced PGC-1α acetylation, and SIRT1 inhibition abrogated FGF18-mediated protective effects. Collectively, FGF18 attenuates rat myocardial MIRI by alleviating oxidative stress and regulating mitochondrial homeostasis through SIRT1-mediated deacetylation of PGC-1α.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"389-400"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148260898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Lipid Metabolism-Related Gene <i>GM2A</i> as a Potential Biomarker in Atopic Dermatitis by Combining Weighted Gene Co-Expression Network Analysis and Machine Learning.","authors":"Lin Wang, Yan-Hong Mao, Li-Tao Zhang","doi":"10.1177/10445498261449596","DOIUrl":"10.1177/10445498261449596","url":null,"abstract":"<p><p>Lipid metabolism is abnormal in patients with atopic dermatitis (AD). This study aimed to screen lipid metabolism-related gene (LMRG) in AD, providing insights into the underlying mechanisms of lipid metabolism abnormalities in AD. Gene expression profiles from the Gene Expression Omnibus were analyzed to identify a hub LMRG in AD through an integrative approach combining weighted gene co-expression network analysis, differential expression analysis, and machine learning. The diagnostic value of the hub gene was assessed by receiver operating characteristic curve analysis. Its biological functions and associations with immune cells were investigated using Gene Set Enrichment Analysis (GSEA)/GSVA and ssGSEA/correlation analysis, respectively. The expression of ganglioside GM2 activator (<i>GM2A</i>) in clinical samples was measured using reverse transcription quantitative polymerase chain reaction and an ELISA assay. We identified 14 LMRGs that were differentially expressed between AD and normal samples and were correlated with AD onset. By three machine learning algorithms, <i>GM2A</i> was identified as a robust LMRG in AD. <i>GM2A</i> expression was observed to be elevated in AD samples across transcriptomic analyses and clinical validation. Moreover, <i>GM2A</i> might be effective in distinguishing between individuals with AD and those without. We further discovered that <i>GM2A</i> was associated with immunomodulation, inflammatory response, and biosynthesis of unsaturated fatty acid pathways. <i>GM2A</i> expression was positively correlated with follicular helper T cells, Activated CD4⁺ T cells, and natural killer T cells. Besides, there was a significant relationship between <i>GM2A</i> and multiple drugs. This study highlighted the significant up-regulation of <i>GM2A</i> as an efficient biomarker for AD, linking it to immune and inflammatory responses as well as immune cell infiltration.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"401-414"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148007528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycosyltransferases as Oncogenic Drivers: Lessons from Cancer Genome Mining.","authors":"Pranoy Sahu, Francesco Russo, Domenico Russo, Alberto Luini, Seetharaman Parashuraman","doi":"10.1177/10445498261450955","DOIUrl":"10.1177/10445498261450955","url":null,"abstract":"<p><p>Glycosylation, the enzymatic addition of sugar chains to proteins and lipids, is the most abundant and chemically diverse form of post-translational modification in eukaryotes. Despite its central role in cell biology, the glycosylation machinery has long been overlooked as a potential driver of cancer. By systematically mining large-scale cancer genomic datasets for somatic copy number alterations, we identified glycosyltransferases as a new class of oncogenic amplification targets. Here we discuss the biological rationale for why alterations in glycosyltransferase genes can drive oncogenesis, the role of the Golgi apparatus as the organizing hub of glycan biosynthesis, and the emerging therapeutic implications of these findings. Collectively, this evidence positions the glycosylation machinery not merely as a bystander altered in malignancy, but as an active and targetable driver of cancer.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"367-372"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148201689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Innate Immune Protein IFITM3 as a γ-Secretase Modulatory Protein: From Inflammation to Alzheimer's Disease.","authors":"Jee-Soo Choi, Ji-Yeun Hur","doi":"10.1177/10445498261456523","DOIUrl":"10.1177/10445498261456523","url":null,"abstract":"<p><p>The mechanisms of Alzheimer's disease (AD) development are complex, and the detailed roles of neuroinflammation in AD still need to be elucidated. With various genetic and environmental risk factors, the accumulation of harmful amyloid plaques containing amyloid-β (Aβ) peptides is one of the main hallmarks of AD. Recent findings show that the innate immune protein interferon-induced transmembrane protein 3 (IFITM3) binds to γ-secretase and modulates Aβ production, providing a direct link between neuroinflammation, amyloidogenesis, and the pathogenesis of AD. In this review, we explore IFITM3-mediated modulation of γ-secretase complex activity and its pivotal role in AD pathology during neuroinflammation. Furthermore, we also provide an overview of the recent growing evidence connecting the roles of infection, the immune system, and AD pathogenesis.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"381-388"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148207368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing Long Noncoding RNA <i>CRNDE</i> Alleviates Hypoxia-Induced Myocardial Cell Injury by Inhibiting the NLRP3/ASC Pathway.","authors":"Zhenwei Xu, Yayi Huang, Hebin Chen, Zhiming Ye, Yanlong Huang, Jingfa Zhu","doi":"10.1177/10445498261454150","DOIUrl":"10.1177/10445498261454150","url":null,"abstract":"<p><p>Myocardial ischemia-induced cell injury involves the concurrent occurrence of pyroptosis, apoptosis, and oxidative stress, whereas its upstream regulatory mechanism remains unclear. The present study aimed to investigate the functional association between long noncoding RNA <i>CRNDE</i> and the NLRP3/ASC pathway in H9c2 cardiomyocytes subjected to hypoxia-induced injury. Using H9c2 cardiomyocytes as the research model, a hypoxia-induced injury model was constructed, shRNA-mediated knockdown of <i>CRNDE</i> was performed, and functional rescue experiments were conducted in combination with an NLRP3 agonist. Results showed that hypoxia treatment significantly upregulated the expression level of <i>CRNDE</i> in H9c2 cells, and this upregulation was significantly positively correlated with the activation of the NLRP3/ASC pathway. Knockdown of <i>CRNDE</i> specifically inhibited the mRNA and protein expression of key molecules in the NLRP3/ASC pathway (NLRP3, ASC, Caspase-1, GSDMD); reduced the secretion of inflammatory factors IL-1β and IL-18; decreased the cell apoptosis rate; and improved oxidative stress imbalance. RNA FISH assay confirmed that <i>CRNDE</i> was localized in the cytoplasm of H9c2 cells; knockdown of <i>CRNDE</i> alleviated hypoxia-induced mitochondrial damage, G1/S phase cell cycle arrest, and impairment of cell membrane integrity, and the above protective effects could be reversed by the NLRP3 agonist. In conclusion, <i>CRNDE</i> is closely associated with hypoxia-induced cardiomyocyte injury, and its effects in mediating pyroptosis, apoptosis, and oxidative stress rely on activation of the NLRP3/ASC pathway. Targeting <i>CRNDE</i> may provide a supplementary strategy for the treatment of myocardial ischemia-related diseases.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"415-425"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148255053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Essential Role for XRCC1 and PARP1 in the Repair of Genotoxic Damage During Spermatogenesis.","authors":"Emad A Ahmed","doi":"10.1177/10445498261456504","DOIUrl":"10.1177/10445498261456504","url":null,"abstract":"<p><p>X-ray repair cross-complementing protein 1 (XRCC1) protects cells from the effects of genotoxic stress by coordinating base excision repair (BER) and DNA single-strand break repair. XRCC1 phosphorylation and recruitment to sites of DNA damage are dependent on poly(ADP-ribose) polymerase-1 (PARP1) activity. As a central scaffolding protein, XRCC1 interacts with multiple components of BER pathway and also contributes to DNA double-strand break repair through the alternative nonhomologous end-joining pathway. In this regard, both established and recent studies have highlighted its critical role in spermatogenesis, extending beyond its classical association with PARP1. By integrating expression profiles with functional evidence, this review summarizes current insights into XRCC1 expression and subnuclear localization in spermatogenic cells, as well as its cooperative interaction with PARP1 in maintaining genomic integrity through efficient recombination and repair of genotoxic damage.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"373-380"},"PeriodicalIF":2.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148177445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intervention Study on the Regulation of circAno6/miR-296-3p/TLR4 Signaling Axis by Shugan Jianpi Formula to Alleviate Inflammation Cascade and Inhibit HSC Activation.","authors":"Qian Wu, Tingting Li, Jing Qu, Chang Fan, Lili Zhang, Hui Jiang","doi":"10.1177/10445498261442830","DOIUrl":"10.1177/10445498261442830","url":null,"abstract":"<p><p>Liver fibrosis (LF) is a fibrotic and inflammatory condition resulting from chronic liver damage, and the activation of hepatic stellate cells (HSCs) is the central event. Our prior research has revealed that the circAno6/miR-296-3p/Toll-like receptor (TLR4) pathway is a key signaling axis in the pathogenesis of LF. Shugan Jianpi Formula (SGJPF) is a traditional Chinese medicinal treatment widely used to treat LF. We hypothesized that SGJPF exerts anti-LF effects by modulating the circAno6/miR-296-3p/TLR4 signaling axis, attenuating inflammatory responses, and inhibiting HSC activation, thereby ultimately mitigating LF. In this study, an SGJPF extraction solution was first prepared and administered to rats via gavage at a specified dosage. Blood samples were subsequently collected from the abdominal aorta to prepare SGJPF-containing serum. Optimal SGJPF intervention conditions were determined using the Cell Counting Kit-8 assay. Flow cytometry was used to assess JS-1 cell cycle progression. The levels of interleukin-1 beta (IL-1β) and IL-18 were measured by enzyme-linked immunosorbent assay. The expression levels of collagen type I (collagen I), α-smooth muscle actin (α-SMA), circAno6, TLR4, miR-296-3p, and NOD-like receptor protein 3 (NLRP3) were evaluated using Western blotting, immunofluorescence, and real-time quantitative polymerase chain reaction. The results indicated that the optimal intervention condition involved serum containing 20% SGJPF, which was administered for a duration of 48 h. SGJPF-containing serum has been shown to reduce the viability of JS-1 cells and decrease the cell count in the G2 + S phase, thereby affecting HSC function. Furthermore, SGJPF-containing serum effectively suppressed the expression levels of NLRP3, IL-1β, IL-18, collagen I, α-SMA, circAno6, and TLR4 while upregulating miR-296-3p expression. These findings suggest that SGJPF can modulate the activity of the circAno6/miR-296-3p/TLR4 signaling axis, attenuate inflammatory responses, and inhibit HSC activation, thereby mitigating LF.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"351-360"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147730977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SUMOylation in Neural Health and Disease: From Cellular Homeostasis to Neurodegeneration.","authors":"Ghaleb Oriquat, Ihsan K Jasim, Tushar B Gajjar, Malathi Hanumanthayya, Israa Abdulhameed Ahmad, Gunjan Singh, Laxmidhar Maharana, Neeraj Bainsal","doi":"10.1177/10445498261444640","DOIUrl":"10.1177/10445498261444640","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDDs) represent a growing global health burden, particularly in aging populations. These disorders primarily affect neurons and are characterized by progressive neuronal dysfunction and loss within specific regions of the central nervous system. Major NDDs include Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, multiple sclerosis, and stroke. Although each disorder exhibits distinct genetic backgrounds and pathological protein aggregates, they share common pathogenic mechanisms, including chronic neuroinflammation, impaired autophagy and mitophagy, disrupted proteostasis, telomere instability, and epigenetic alterations. A hallmark feature across NDDs is the accumulation of misfolded proteins, leading to synaptic dysfunction and neuronal degeneration. Small ubiquitin-like modifiers (SUMOs) are a family of ∼100 amino acid proteins, including SUMO1 and the closely related SUMO2/3 isoforms. SUMOylation is a dynamic posttranslational modification that regulates protein function through the covalent attachment or removal of SUMO moieties. This reversible process is mediated by SUMO-specific E1 activating, E2 conjugating, and E3 ligating enzymes and is counterbalanced by SUMO/Sentrin-specific proteases. The SUMOylation status of target proteins depends on the tightly controlled balance between conjugation and deconjugation systems. Acting as a molecular switch, SUMOylation modulates diverse cellular processes such as DNA damage repair, RNA metabolism, transcriptional regulation, and protein quality control, all of which are essential for maintaining cellular homeostasis. Accumulating evidence links dysregulated SUMOylation to the pathogenesis of multiple neurological disorders, including polyglutamine and synucleinopathies. SUMOylation influences neuroinflammation, oxidative stress, protein aggregation, neuroangiogenesis, ischemic injury, and demyelination. This review highlights recent advances in understanding the role of SUMOylation in NDDs and explores its potential as a promising therapeutic target.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"299-316"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Impact of Homeopathic Medicines on Dental Stem Cells: An Experimental Study.","authors":"Marli Cristina Pereira, Thainá Beatriz Soares, Jeferson Luis de Oliveira Stroparo, Sabrina Cunha da Fonseca, Lisley Janowski Spisila, Leila Mourão, Rosy de Oliveira Nardi, Carla Castiglia Gonzaga, Célia Regina Cavichiolo Franco, Moira Pedroso Leão, Katia Raquel Weber, Carolina Maria Costa de Oliveira Souza, Daiany de Souza Dobuchak, Thiago Macedo de Lima Mariano, João César Zielak","doi":"10.1177/10445498261444142","DOIUrl":"10.1177/10445498261444142","url":null,"abstract":"<p><p>This study investigated the influence of homeopathic medicines (HMs) on the <i>in vitro</i> behavior of stem cells from human exfoliated deciduous teeth (SHED). The HMs <i>Symphytum officinale</i> (SO), <i>Calcarea carbonica</i> (CC), and <i>Calcarea phosphorica</i> (CP) were evaluated, along with a vehicle control (V), using cells from a single donor in passages 4 (P4) and 5 (P5). Cellular responses were assessed using Neutral Red (viability-related activity), Crystal Violet (adherent cell density), MTT (metabolic activity), and scanning electron microscopy (SEM). Across assays, consistent modulation of cellular behavior was observed, particularly in P5 at 72 h. Neutral Red uptake increased over time in P4 and showed treatment-dependent responses in P5. Crystal Violet indicated increased adherent cell density, with higher values in P5 compared to P4. MTT demonstrated increased metabolic activity at 72 h, especially in P5. SEM analysis confirmed these findings, showing that cells treated with SO, CC, and CP remained well adhered and spread, with increased cell density and more compact organization. In contrast, the vehicle group exhibited reduced cell density and altered morphology. Overall, the tested HMs were associated with measurable changes in SHED behavior without evident adverse effects. These findings should be interpreted as exploratory and require further validation.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"343-350"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147730988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}