Frontiers in Molecular Biosciences最新文献

{"title":"Editorial: Understanding the mechanism of dynamic cell communications: a much needed angle for cell motility and barrier functions.","authors":"Virag Vas, Zhen Xu, Pasquale Cervero","doi":"10.3389/fmolb.2025.1663453","DOIUrl":"10.3389/fmolb.2025.1663453","url":null,"abstract":"","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1663453"},"PeriodicalIF":3.9,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12331756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144816230","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":"Cerium oxide nanoparticles attenuates fibrosis and inflammation in thyroid-associated ophthalmopathy via JNK pathway.","authors":"Bo-Wen Wang, Ru Zhu, Ying Jin, Xuan Ouyang, Fa-Gang Jiang, Xing-Hua Wang","doi":"10.3389/fmolb.2025.1580062","DOIUrl":"10.3389/fmolb.2025.1580062","url":null,"abstract":"<p><strong>Objective: </strong>Thyroid-associated ophthalmopathy (TAO) is an autoimmune orbital disorder characterized by pathological alterations including extraocular muscle fibrosis and orbital inflammation. Cerium oxide nanoparticles (CeO2-NPs, CNPs) are gaining popularity in ophthalmology due to their potential antifibrotic and anti-inflammatory properties. This study aims to investigate the inhibitory effects of CNPs on fibrosis and inflammation in TAO orbital fibroblasts (OFs) derived from TAO patients.</p><p><strong>Methods: </strong>OFs obtained by primary culture of orbital adipose tissue from 8 TAO patients. Probing the safe action concentration of CNPs and Anisomycin using CCK8 and detecting intracellular reactive oxygen species (ROS) generation using ROS Assay kit. Wound-Healing Assay was used to examine the degree of fibrosis of OFs. The expression of Fibronectin, COL1A1, α-Smooth muscle action, Hyaluronan Synthase 2, c-Jun N-terminal Kinase (JNK) and pJNK were detected by the RT-PCR and WB, and Hyaluronic Acid secretion was detected by ELISA. Inflammatory factors Interleukin-6 (IL-6) and Tumor Necrosis Factor-α (TNFα) expression were detected by RT-PCR and ELISA.</p><p><strong>Results: </strong>CNPs below 100 μg/mL and Anisomycin below 5 μM did not affect OFs proliferation. CNPs inhibit intracellular ROS generation. CNPs inhibit OFs fibrosis and suppress the expression of fibrosis indicators. These antifibrotic effects were mediated by inhibition of JNK phosphorylation, and were reversible by a JNK agonist. Furthermore, CNPs reduce both mRNA levels and secretion of inflammatory factors, IL-6 and TNF-α.</p><p><strong>Conclusion: </strong>CNPs demonstrated the ability to inhibit fibrosis in TAO OFs by reducing JNK phosphorylation, as well as dose-dependently suppressed ROS generation and inflammatory response in TAO OFs.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1580062"},"PeriodicalIF":3.9,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12325074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793929","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":"Maternal plasma microRNA profiles in twin-twin transfusion syndrome and normal monochorionic twin pregnancies.","authors":"Steven T Papastefan, Morgan M Langereis, Catherine R Redden, Daniel R Liesman, Cassandra B Huerta, Lucas E Turner, Hee Kap Kang, Bethany T Stetson, Katherine C Ott, William S Marriott, Joyceline A S Ito, Aimen F Shaaban, Amir M Alhajjat","doi":"10.3389/fmolb.2025.1597215","DOIUrl":"10.3389/fmolb.2025.1597215","url":null,"abstract":"<p><strong>Introduction: </strong>Ultrasound-based staging systems for twin-twin transfusion syndrome (TTTS) are limited by radiologic expertise, fetal positioning, and timing of the exam, and may benefit from incorporation of objective biochemical measures for diagnosis and prognostication. microRNA expression is altered in amniotic fluid of TTTS patients, however the invasive nature of amniocentesis has precluded practical incorporation of these biomarkers into current staging systems. Therefore, we sought to assess whether non-invasive maternal plasma microRNAs can distinguish between TTTS and normal monochorionic diamniotic (MCDA) twin pregnancies.</p><p><strong>Methods: </strong>Maternal blood samples were collected for patients with normal MCDA twin pregnancies (n = 11) or prior to selective fetoscopic laser photocoagulation (SFLP) for patients with TTTS (n = 36). Extracted microRNA from a panel of 24 microRNAs was compared between groups.</p><p><strong>Results: </strong>miR-26a-5p (P = 0.004), miR-222-3p (P = 0.007), and miR-145-5p (P = 0.047) were downregulated and miR-320a-3p (P = 0.005) was upregulated in the maternal plasma of TTTS patients compared to controls. miR-26a-5p, miR-320a-3p, and miR-222-3p in combination were strong predictors of TTTS on random forest modeling (area under curve = 0.905). After SFLP, all significantly dysregulated microRNAs in TTTS trended toward levels of expression observed in control MCDA twin pregnancies.</p><p><strong>Conclusion: </strong>Several microRNAs are differentially expressed in maternal plasma and demonstrate strong predictive capacity for identifying twin-twin transfusion syndrome. These plasma microRNAs could provide minimally invasive means to enhance currently established ultrasound diagnostic criteria for twin-twin transfusion syndrome.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1597215"},"PeriodicalIF":3.9,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12325072/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793930","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":"TOP2A as a prognostic biomarker in small cell carcinoma of the esophagus: an integrated bioinformatics and immunohistochemical study.","authors":"Xiaolei Yin, Xiaopeng Li, Lili Mi, Jiaojiao Hou, Fei Yin","doi":"10.3389/fmolb.2025.1640881","DOIUrl":"10.3389/fmolb.2025.1640881","url":null,"abstract":"<p><strong>Background: </strong>Small cell carcinoma of the esophagus (SCCE) is an infrequent but highly aggressive cancer with a poor prognosis. Given its low incidence, there is a lack of validated biomarkers to guide risk stratification and inform treatment decisions.</p><p><strong>Methods: </strong>We extracted Differentially expressed genes (DEGs) from the GSE111044 dataset using standard bioinformatics workflows. A network of interacting proteins was assembled to determine hub genes, and TOP2A and CDK1 were selected for immunohistochemical (IHC) validation in 76 SCCE tumor samples. IHC staining scores were analyzed for associations with clinicopathological features. Survival analysis was conducted using Kaplan-Meier estimations and Cox regression modeling to pinpoint independent prognostic factors. To further assess the clinical utility, TOP2A expression was combined with VALSG staging for risk stratification.</p><p><strong>Results: </strong>A comparison between SCCE and adjacent normal tissues revealed 1,202 DEGs. PPI network analysis highlighted two hub genes, TOP2A and CDK1, which IHC validated in 76 SCCE samples. High TOP2A expression was significantly associated with advanced TNM stage (p = 0.020) and deeper tumor invasion (p = 0.004). Multivariate Cox analysis identified high TOP2A expression (HR = 1.92, 95% CI: 1.30-2.82, p = 0.001) and VALSG stage (HR = 2.20, 95% CI: 1.07-4.50, p = 0.031) as independent predictors of prognosis. Time-dependent ROC analysis indicated that the AUCs for the VALSG stage alone were 0.626, 0.638, and 0.602 at 1-, 2-, and 3-year time intervals, respectively. TOP2A alone yielded slightly higher AUCs of 0.719, 0.632, and 0.676. Notably, the combination of TOP2A and VALSG provided the greatest predictive accuracy, achieving AUCs recorded at 0.721, 0.734, and 0.773 at the respective time points.</p><p><strong>Conclusion: </strong>This study suggests that TOP2A is a novel, independent prognostic biomarker in SCCE. When integrated with the VALSG staging system, TOP2A expression enhances risk stratification and may serve as a useful adjunct in clinical prognostication. These findings support its clinical utility while emphasizing the necessity for future studies to include prospective validation.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1640881"},"PeriodicalIF":3.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12321555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788686","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":"Deuterium trafficking, mitochondrial dysfunction, copper homeostasis, and neurodegenerative disease.","authors":"Stephanie Seneff, Anthony M Kyriakopoulos","doi":"10.3389/fmolb.2025.1639327","DOIUrl":"10.3389/fmolb.2025.1639327","url":null,"abstract":"<p><p>Deuterium is a natural heavy isotope of hydrogen, containing an extra neutron. Eukaryotic organisms have devised complex metabolic policies that restrict the amount of deuterium reaching the mitochondria, because it damages the ATPase pumps, leading to release of excessive reactive oxygen species and inefficiencies in ATP production. Human metabolism relies heavily on the gut microbiome to assure an abundant supply of deuterium depleted (deupleted) nutrients to the host. Mitochondrial dysfunction is a hallmark of many chronic diseases, and deuterium overload, often due to gut dysbiosis, may be a major factor contributing to this issue. In this paper, we explore the potential role of certain amyloidogenic proteins, including amylin, amyloid beta, the prion protein, huntingtin, and <i>α</i>-synuclein, in disease processes that result in the accumulation of deposits of protein fibrils, along with lipid membrane components of damaged mitochondria, which we argue may be a mechanism to sequester deuterium in order to reduce the deuterium burden in the tissues. We show how cardiolipin, an anionic lipid synthesized in mitochondria and localized to the mitochondrial membrane, may play a central role both in trapping deuterium in the mitochondrial membrane and in inducing protein misfolding to facilitate the formation of deuterium-rich deposits. We focus on the potential role of the amino acid histidine and its interaction with the mineral copper, both to catalyze certain essential reactions and to facilitate the misfolding of amyloidogenic proteins triggered by contact with anionic phospholipids, particularly cardiolipin, and especially in the outer mitochondrial membrane of deuterium-damaged mitochondria.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1639327"},"PeriodicalIF":3.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12322706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788685","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":"RNA sequencing-based profiling of differentially expressed microRNAs in endothelial cells from offspring of hypertensive pregnancies: a preliminary study.","authors":"Nurul Iffah Mohd Isa, Aslah Nabilah Abdull Sukor, Saiful Effendi Syafruddin, Mohd Faizal Ahmad, Shahidee Zainal Abidin, Mohd Helmy Mokhtar, Azizah Ugusman, Adila A Hamid","doi":"10.3389/fmolb.2025.1520101","DOIUrl":"10.3389/fmolb.2025.1520101","url":null,"abstract":"<p><p>Offspring of mothers with hypertensive disorders of pregnancy (HDP) are at increased risk of developing endothelial dysfunction and cardiovascular disease (CVD) in adulthood. MicroRNAs (miRNAs), as key regulators of endothelial cells, may contribute to the early onset of endothelial dysfunction. However, there are limited studies characterizing the miRNA profile of endothelial cells in offspring of HDP. Therefore, this study aims to determine the miRNA expression profile of human umbilical vein endothelial cells (HUVECs) isolated from the offspring of HDP. HUVECs were obtained from both normal and hypertensive umbilical cords. RNA sequencing analysis revealed that eight miRNAs were significantly upregulated in HUVECs from HDP (p < 0.05). The target genes of these miRNAs were then predicted using four databases: miRDB, TargetScan, DIANA-microT-CDS, and miRWalk. Gene ontology, pathway enrichment, and protein-protein interaction network analyses revealed that the target genes of these miRNAs are involved in cellular functions and pathways related to angiogenesis and cellular senescence, which may contribute to endothelial dysfunction and CVD. The most significantly upregulated miRNA, hsa-miR-196a-5p expression was then validated through stem-loop RT-qPCR where its expression was significantly upregulated in hypertensive HUVEC by 6-fold as compared to normal HUVEC (p < 0.01). These findings offer insights into the role of miRNAs in the development of CVD in offspring exposed to HDP, highlighting their potential as predictive markers and therapeutic targets in the future.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1520101"},"PeriodicalIF":3.9,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12391922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144949032","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":"Dynamic contrast-enhanced MRI-based radiomics model of intra-tumoral kinetic heterogeneity for predicting breast cancer molecular subtypes.","authors":"Yue Cheng, Ran Ren, Yu Xu, Shaofeng Duan, Jilei Zhang, Zhongyuan Bao","doi":"10.3389/fmolb.2025.1635296","DOIUrl":"10.3389/fmolb.2025.1635296","url":null,"abstract":"<p><strong>Objectives: </strong>This study aims to segment intra-tumoral subregions of breast cancer based on kinetic heterogeneity using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). It also aims to construct a radiomics model of the whole tumor and washout region to predict molecular subtypes and human epidermal growth factor receptor 2 (HER2) status.</p><p><strong>Methods: </strong>A total of 124 patients with biopsy-confirmed breast cancer were randomly divided into training and test sets in a 7:3 ratio. Quantitative analysis of breast cancer kinetic heterogeneity parameters based on DCE-MRI data was performed, dividing tumors into three subregions (Persistent, Washout, and Plateau) according to the type of voxel-level contrast enhancement. Radiomics features of the washout region and the whole tumor were extracted from the first phase of DCE-MRI enhancement. The area under the receiver operating characteristic curve (AUC) and decision curve analysis (DCA) were used to evaluate the performance of the model.</p><p><strong>Results: </strong>The radiomics model using tumor subregion (washout region) features related to kinetic heterogeneity showed the best performance for differentiating between patients with Luminal, HER2, and HER2 status, with AUC values in the train set of 0.924, 0.876, and 0.816, respectively. Exhibiting an AUC value higher than that obtained with the whole tumor and the kinetic heterogeneity parameters. DCA curves showed that the washout region model was more effective in predicting Luminal and HER2-status subtypes, compared to the whole tumor region model.</p><p><strong>Conclusion: </strong>Radiomics analysis of washout areas from high-resolution DCE-MRI breast scans has the potential to better identify molecular subtypes of breast cancer non-invasively.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1635296"},"PeriodicalIF":3.9,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12313481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775074","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":"Proteomic and structural comparison between cilia from primary ciliary dyskinesia patients with a DNAH5 defect.","authors":"Charlotte de Ceuninck van Capelle, Leo Luo, Alexander Leitner, Stefan A Tschanz, Philipp Latzin, Sebastian Ott, Tobias Herren, Loretta Müller, Takashi Ishikawa","doi":"10.3389/fmolb.2025.1593810","DOIUrl":"10.3389/fmolb.2025.1593810","url":null,"abstract":"<p><strong>Introduction: </strong>Primary ciliary dyskinesia (PCD) is a genetic disorder affecting motile cilia across various organs, leading to recurrent respiratory infections, subfertility, and laterality defects. While several diagnostic tools exist-such as high-speed video microscopy, immunofluorescence staining, electron microscopy, and genetic screening-the relationship between different pathogenic variants within a single PCD gene and their effects on ciliary composition, structure, and clinical phenotype remains poorly understood.</p><p><strong>Methods: </strong>To investigate this, we analyzed cilia from PCD patients with different mutations in axonemal dynein heavy chain <i>dnah5</i> using mass spectrometry and cryo-electron tomography. These methods allowed us to examine both the protein composition and ultrastructural organization of motile cilia in affected individuals.</p><p><strong>Results: </strong>Though all analyzed patients present similarly in traditional diagnostic methods, we observed differences in axonemal composition among patients carrying different <i>dnah5</i> mutations. Specific reductions in ciliary components varied between individuals, indicating a mutation-specific impact. Notably, proteins such as VWA3B, KIAA1430/CFAP97, and DTHD1-not previously identified as components of human respiratory motile cilia-were detected in wild type cilia, but not in patient cilia. Lastly, we confirmed some changes in protein abundance in the 96-nm repeated unit of the axoneme between wild-type and PCD samples.</p><p><strong>Discussion: </strong>These findings suggest that mutations in <i>dnah5</i> result in varied and specific alterations in axonemal composition, reflecting the heterogeneity of the disease at the molecular level. The discovery of novel ciliary proteins and mutation-specific differences enhances our understanding of the complexity of PCD pathogenesis and may inform future diagnostic and therapeutic strategies.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1593810"},"PeriodicalIF":3.9,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12310455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759633","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":"Development of a human colorectal carcinoma cell-based platform for studying inducible nitric oxide synthase expression and nitric oxide signaling dynamics.","authors":"Xi Chen, Elizabeth A Grimm, Yong Qin","doi":"10.3389/fmolb.2025.1637230","DOIUrl":"10.3389/fmolb.2025.1637230","url":null,"abstract":"<p><strong>Introduction: </strong>Inducible nitric oxide synthase (iNOS) plays a critical role in inflammatory signaling and tumor immunology, contributing to both pro- and anti-tumor effects depending on the cellular context. While iNOS induction has been linked to immune activation and tumor progression, its expression in cancer cells is highly variable and often inconsistently reported across different tumor models. To address this gap, we developed a well-defined <i>in vitro</i> platform using the human colorectal adenocarcinoma cell line DLD-1 to model stimulus-dependent iNOS expression and nitric oxide (NO) signaling.</p><p><strong>Methods: </strong>DLD-1 cells were stimulated with a pro-inflammatory cytokine cocktail (lipopolysaccharide [LPS], interleukin-1β [IL-1β], and interferon-γ [IFN-γ]), resulting in marked upregulation of iNOS at both the mRNA and protein levels. iNOS specificity was confirmed using targeted siRNA knockdown. Functional assessment of NO production was performed using the Nitrate/Nitrite Colorimetric Assay Kit and the ENO-30 NOx Analyzer. Induction of iNOS was further associated with elevated levels of reactive nitrogen species (RNS), reactive oxygen species (ROS), and protein nitration, including 3-nitrotyrosine, detected by immunohistochemistry and Western blot.</p><p><strong>Results: </strong>Upon stimulation, DLD-1 cells consistently expressed enzymatically active, full-length human iNOS and produced biologically relevant levels of NO and downstream nitrosative stress markers. Treatment with selective iNOS inhibitors significantly reduced nitrite accumulation, confirming the functional activity of iNOS and the model's applicability for pharmacologic evaluation of NO-modulatory compounds.</p><p><strong>Discussion: </strong>Our findings establish the DLD-1 cell line as a reproducible and well-controlled in vitro system for studying inducible iNOS expression and downstream NO/RNS signaling in human epithelial cancer cells. This platform provides a valuable tool for mechanistic studies, screening of iNOS-targeted agents, and resolving discrepancies in iNOS detection across experimental models in cancer biology.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1637230"},"PeriodicalIF":3.9,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12310501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759632","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":"The role of epigenetics in pulmonary fibrosis: recent advances in mechanistic insights and therapeutic implications.","authors":"Jingru Huang, Jianfeng Qin, Yuguang Zhu, Ao Shen","doi":"10.3389/fmolb.2025.1647300","DOIUrl":"10.3389/fmolb.2025.1647300","url":null,"abstract":"<p><p>Pulmonary fibrosis (PF) is a fatal disease characterized by progressive fibrosis of lung tissue, with a key pathological feature of excessive accumulation of extracellular matrix. PF occurs from complicated origins, while emerging findings have suggested the involvement of the environmental factors in the risk of PF through epigenetic regulation. This article will discuss how recent advances in epigenetic alterations of DNA methylation, RNA methylation, histone modifications, and non-coding RNAs contribute to PF development through molecular mechanisms and cellular processes, including fibroblast-to-myofibroblast transition (FMT), epithelial-to-mesenchymal transition (EMT), alveolar epithelial cell injury and immune cell interactions in the past 5 years.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1647300"},"PeriodicalIF":3.9,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12310491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759634","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}