Frontiers in Cell and Developmental Biology最新文献

{"title":"Hippo-YAP/TAZ signaling in inner ear development, injury, and regeneration: evidence synthesis and the biomechanical brake hypothesis.","authors":"Dongmei Guan, Xinghong Liu, Xiaoyi Zhang, Jingqi Zhang, Hui Xie","doi":"10.3389/fcell.2026.1878367","DOIUrl":"10.3389/fcell.2026.1878367","url":null,"abstract":"<p><p>Sensorineural hearing loss in mammals is essentially irreversible. Mature cochlear hair cells, once lost, do not regenerate. Non-mammalian vertebrates retain this ability, but in the mammalian organ of Corti, supporting cells lose their proliferative and transdifferentiation competence after birth. Reactivation of classical developmental pathways has also shown limited success in the adult cochlea. In this review, we first synthesize published evidence on Hippo-Yes-associated protein(YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) signaling in the inner ear, including studies of inner-ear progenitors, organ of Corti growth, vestibular sensory epithelia, cochlear hair-cell injury, neonatal cochlear regeneration models, and emerging adult cochlear data. On this basis, we then evaluate the biomechanical brake hypothesis, which proposes that injury-associated mechanical remodeling may interact with Hippo-YAP/TAZ signaling to restrict supporting-cell plasticity in the mature mammalian cochlea. Rather than presenting this hypothesis as an established mechanism, we treat it as an evidence-graded framework that must be tested against alternative explanations, including protective epithelial repair, cell-cycle inhibition, epigenetic restriction, and loss of developmental competence. The available literature suggests that Hippo-YAP/TAZ signaling participates in several inner-ear processes, including progenitor expansion, sensory epithelial growth, species-dependent vestibular repair, otoprotective responses, and supporting-cell proliferation under defined experimental conditions. However, direct evidence that injury-induced mechanical remodeling causally suppresses YAP/TAZ-dependent regeneration in the adult cochlea remains limited. We therefore distinguish among developmental, neonatal, vestibular, <i>ex vivo</i>, and adult <i>in vivo</i> evidence, and identify where current findings support, weaken, or remain insufficient to establish the biomechanical brake model. Finally, we outline specific gaps that should guide future work: comprehensive tabulation of Hippo-related inner-ear studies, adult supporting-cell lineage tracing, spatial mapping of cochlear mechanical properties and Hippo activity, cell-subtype-specific perturbation of YAP/TAZ signaling, functional assessment by auditory brainstem response and distortion product otoacoustic emission, and long-term evaluation of epithelial stability. This organization is intended to clarify what Hippo-YAP/TAZ signaling has already been shown to do in the inner ear, what remains speculative, and which experiments are required before mechanobiological modulation can be considered a plausible regenerative strategy.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1878367"},"PeriodicalIF":5.3,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Iron, lipid peroxidation and discogenic pain: a redox framework for ferroptosis in intervertebral disc degeneration.","authors":"Qiyun Shi, Xiaotong Xu, Shen Zhai, Jitian Li, Yongwei Song","doi":"10.3389/fcell.2026.1938559","DOIUrl":"10.3389/fcell.2026.1938559","url":null,"abstract":"<p><p>The weak correlation between radiographic disc degeneration and pain intensity remains unresolved in intervertebral disc degeneration (IVDD). This Review proposes that iron-dependent lipid peroxidation and ferroptosis-associated redox signalling constitute an underrecognised link between degenerative stress and a pro-nociceptive disc microenvironment. Two linked frameworks are developed. The pro-ferroptotic niche integrates four disc-specific mechanisms: Piezo1-mediated iron influx, ferroportin suppression, ferritinophagy mediated by the cargo receptor NCOA4, and glycolysis-derived lactate upregulating the PUFA-activating enzyme ACSL4. ALOX15-coupled lipid peroxidation rests mainly on cross-disease inference. The ferroptotic pain hub proposes that resulting damage-associated signals, including the alarmin HMGB1 and 4-hydroxynonenal, may converge on NF- <math><mrow><mi>κ</mi></mrow> </math> B-dependent induction of NGF, BDNF, and IL-6. Relevant receptor-level signalling is supported in disc cells, whereas the ferroptosis-specific coupling remains untested. Intervention is organised into four tiers: iron handling, antioxidant-reserve restoration, lipid-peroxidation blockade, and damage-signal-NF- <math><mrow><mi>κ</mi></mrow> </math> B interruption. Deferoxamine and N-acetylcysteine are discussed as an illustrative, unvalidated multi-tier combination, with translation constrained by the need for disc-adapted delivery, intradiscal pharmacokinetic/pharmacodynamic characterisation, local safety assessment, and pain-endpoint validation. Disc-specific evidence, cross-disease inference, mechanistic inference, and hypothesis-level prediction are distinguished throughout, with falsifiable tests defined. The aim is not to present ferroptosis as a proven cause of discogenic pain, but to offer a testable framework for mechanism-based stratification of painful IVDD.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1938559"},"PeriodicalIF":5.3,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642720/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics integration identifies Acsm2/ACSM2A deficiency as a metabolic driver of ZBP1-mediated PANoptosis in acute kidney injury.","authors":"Lijuan Lu, Yuping Qin","doi":"10.3389/fcell.2026.1936504","DOIUrl":"10.3389/fcell.2026.1936504","url":null,"abstract":"<p><p>Acute kidney injury (AKI) converges on tubular epithelial cell (TEC) death and metabolic collapse, fueling the transition to chronic kidney disease (CKD), yet the molecular link between metabolic failure and inflammatory cell death remains poorly defined. Here, we integrated cross-model transcriptomics of three mechanistically distinct murine AKI models with single-cell RNA-seq, high-dimensional weighted gene co-expression network analysis, and machine learning feature selection. This multi-omics framework identified acyl-CoA synthetase medium-chain family member 2 (Acsm2), a rate-limiting mitochondrial enzyme for medium-chain fatty acid β-oxidation, as the top conserved hub gene suppressed in injured proximal tubule cells. Acsm2/ACSM2A downregulation was confirmed in mouse AKI models and in human HK-2 cells subjected to oxygen-glucose deprivation/reperfusion (OGD/R). ACSM2A deficiency alone was sufficient to simultaneously activate apoptosis, pyroptosis, and necroptosis, indicative of PANoptosis, whereas restoration of ACSM2A expression attenuated OGD/R-induced cell death. Mechanistically, <i>ACSM2A</i> loss provoked mitochondrial oxidative stress and drove the accumulation of Z-form nucleic acids. Scavenging mitochondrial reactive oxygen species or silencing ZBP1 rescued cells from <i>ACSM2A</i> knockdown-induced cell death, implicating ZBP1 as a downstream mediator. Collectively, our findings establish <i>ACSM2A</i> loss as a trigger of ZBP1-dependent PANoptosis in TECs and position the ACSM2A-ZBP1 axis as a candidate pathogenic mechanism that warrants further investigation as a potential therapeutic node for intercepting the AKI-to-CKD transition.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1936504"},"PeriodicalIF":5.3,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CauSTI: causal spatial transcriptomic interaction inference for cell-cell communication.","authors":"Hongjie Ji, Yue Huang, Yu Lyu","doi":"10.3389/fcell.2026.1943696","DOIUrl":"10.3389/fcell.2026.1943696","url":null,"abstract":"<p><strong>Introduction: </strong>Cell-cell communication plays a critical role in tissue organization, development, immune regulation, and disease progression. Spatial transcriptomics enables the inference of such communication within the native tissue context. However, existing methods often rely on ligand-receptor co-expression or spatial proximity alone, without explicitly modeling the directional nature of intercellular signaling.</p><p><strong>Methods: </strong>We propose CauSTI, a causal spatial transcriptomic interaction inference framework for identifying direction-specific cell-cell communication. CauSTI integrates spatial neighborhood structure with ligand-receptor-derived causal priors through a causal-prior-guided variational graph autoencoder. Spatial proximity defines the tissue graph, while ligand-receptor evidence provides biologically informed directional constraints. An asymmetric decoder models sender-receiver relationships between ordered cell pairs. The optimization objective jointly incorporates spatial reconstruction, causal-prior consistency, variational regularization, and directional regularization.</p><p><strong>Results: </strong>Experiments on three spatial transcriptomic datasets-seqFISH+, MERSCOPE, and Xenium-demonstrate that CauSTI consistently outperforms representative baseline methods in AUROC, ACC, and AP. Ablation studies further confirm the contributions of causal priors and directional regularization.</p><p><strong>Discussion: </strong>These findings suggest that integrating spatial context with causal priors and explicit directional modeling provides an effective framework for inferring biologically plausible, direction-specific cell-cell communication landscapes from spatial transcriptomic data.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1943696"},"PeriodicalIF":5.3,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From retina to brain: retinal dysfunction and dopaminergic neurodegeneration in <i>Drosophila</i> models of Parkinson's disease.","authors":"Justyna Kadłuczka, Jakub Dymek, Elżbieta Pyza, Milena Damulewicz","doi":"10.3389/fcell.2026.1929128","DOIUrl":"10.3389/fcell.2026.1929128","url":null,"abstract":"<p><p>Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons within the substantia nigra pars compacta. Although PD is primarily defined as a motor disorder, prodromal non-motor symptoms - such as circadian clock desynchronization and sleep disturbances - can emerge years before clinical diagnosis. Increasing evidence suggests that these non-motor manifestations, particularly circadian disruption, may contribute to disease progression. However, it remains unclear whether circadian dysfunction actively drives neurodegeneration or arises as a consequence of ongoing neuronal loss. In this study, we employed genetic models of PD in <i>Drosophila melanogaster</i> to investigate these relationships. Specifically, we examined the effects of <i>parkin</i> (<i>park</i>) silencing and neuronal expression of human α-Synuclein on photoreceptor morphology and function. Furthermore, we assessed whether mitophagy impairment or synucleinopathy confined to the visual system can influence the onset and progression of PD-related phenotypes. Given that sleep fragmentation is a common feature in PD patients, we also analyzed sleep patterns in flies, focusing on sleep duration. In parallel, we evaluated dopaminergic neuron degeneration, with particular emphasis on the protocerebral anterior medial (PAM) cluster, which plays a critical role in the regulation of sleep and locomotor activity. Taken together, our findings highlight the importance of elucidating the interplay between retinal cells disruption and neurodegeneration in deeper parts of the brain in Parkinson's disease.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1929128"},"PeriodicalIF":5.3,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13643024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vision-language semantic guidance and topology refinement for robust retinal vessel segmentation and biomarker analysis in cerebral small vessel disease.","authors":"Shanshan Hua, Tao Chen, Yuwei Mi, Yu Shen, Yisha Li, Jiong Zhang, Yunxin Ji","doi":"10.3389/fcell.2026.1940436","DOIUrl":"10.3389/fcell.2026.1940436","url":null,"abstract":"<p><strong>Background: </strong>Retinal microvascular alterations observed in optical coherence tomography angiography (OCTA) have emerged as promising biomarkers for cerebral small vessel disease (CSVD). However, accurate quantification of OCTA-derived vascular biomarkers remains challenging due to imaging noise, projection artifacts, low contrast, and structural discontinuities, which often lead to unreliable vessel segmentation and distorted vascular topology.</p><p><strong>Purpose: </strong>To address these challenges, we propose SemTopNet, a semantic-topology joint modeling framework for OCTA vessel segmentation.</p><p><strong>Methods: </strong>The proposed framework integrates vision-language semantic guidance, centerline-guided topology refinement, and uncertainty-aware adaptive supervision within a unified architecture. Specifically, semantic embeddings are incorporated to enhance global structural representation, while a centerline-guided topology refinement module explicitly improves vascular continuity and suppresses fragmented predictions. In addition, Monte Carlo dropout-based uncertainty estimation is employed to improve robustness in ambiguous and low signal-to-noise regions.</p><p><strong>Results: </strong>Extensive experiments on a CSVD OCTA dataset demonstrate that SemTopNet consistently outperforms existing convolutional and Transformer-based segmentation methods, achieving the best performance in Dice similarity coefficient (0.8931), clDice (0.9027), Recall (0.9293), and AUC (0.9567). Ablation studies further verify the effectiveness of semantic modeling, topology-aware refinement, and uncertainty-aware supervision. Based on the obtained segmentation results, quantitative retinal vascular biomarkers were further analyzed, revealing significant layer-dependent microvascular alterations in CSVD patients, particularly in the deep vascular complex (DVC).</p><p><strong>Conclusion: </strong>These findings demonstrate that topology-consistent OCTA vessel segmentation is essential for reliable retinal microvascular quantification. The proposed SemTopNet provides a robust framework for OCTA biomarker extraction and retinal-cerebral vascular association analysis in CSVD-related studies.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1940436"},"PeriodicalIF":5.3,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelet-derived growth factor-BB (PDGF-BB): pathophysiological roles and therapeutic implications in aging-related diseases.","authors":"Miao Zheng, Kai Huang, Yuanshi She, Jun Qian, Feng Zhang, Qiaocheng Zhai","doi":"10.3389/fcell.2026.1926050","DOIUrl":"10.3389/fcell.2026.1926050","url":null,"abstract":"<p><p>Platelet-derived growth factor-BB (PDGF-BB), a core functional isoform of the PDGF family, serves as a central regulator of cell proliferation, migration, differentiation, and tissue remodeling. Extensive preclinical and clinical evidence indicates that PDGF-BB expression exhibits profound spatiotemporal heterogeneity during natural aging and across various pathological conditions, including cardiovascular, neurodegenerative, and musculoskeletal diseases, as well as malignancies. Importantly, these dynamic expression patterns are intrinsically linked to disease progression and distinct aging phenotypes. Mechanistically, PDGF-BB initiates complex intracellular signaling cascades-such as the ERK, JNK, PI3K-AKT, and mTOR pathways-via specific engagement with PDGFRα/β dimers. Through these networks, PDGF-BB orchestrates intercellular communication and maintains microenvironmental homeostasis in a highly dose-dependent and cell-type-specific manner. Consequently, pharmacological interventions using small molecules, natural products, and biological agents have demonstrated efficacy in modulating PDGF-BB expression and its downstream signaling, presenting promising therapeutic targets for aging-related disorders and associated tissue damage. This review systematically synthesizes the heterogeneous expression profiles of PDGF-BB across natural aging and diverse disease contexts. We delineate the molecular mechanisms underlying its role in driving senescence and pathological progression, and critically evaluate the translational potential and current limitations of PDGF-BB-targeted therapies. By comprehensively mapping the biological network of PDGF-BB, this review aims to provide a conceptual framework for future basic research and clinical translation.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1926050"},"PeriodicalIF":5.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149106760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Automatic diagnosis of retinoblastoma and quantitative analysis of retinal vascular morphology using deep learning.","authors":"Xinyi Deng, Hui Liu, Yijing Chen, Lijun Shen, Lingzhi Cai","doi":"10.3389/fcell.2026.1962785","DOIUrl":"10.3389/fcell.2026.1962785","url":null,"abstract":"<p><strong>Purpose: </strong>To develop a convolutional neural network-based artificial intelligence identification diagnostic system for ultra-wide field fundus images of retinoblastoma (RB) and quantify its vascular morphology features.</p><p><strong>Methods: </strong>A retrospective study. 183 ultra-wide field fundus images from 54 patients diagnosed with RB were included, along with 250 images of healthy control. Of these, 277 images were used as the training set, 100 images were used as the validation set, and 56 images were used for the performance test. A deep learning based on DenseNet was used to train the AI auto-diagnostic network for RB. After manual labelling to remove the lesion area, the binary skeleton vessels of the retina were automatically extracted and segmented. Vascular morphological characteristics were subsequently assessed quantitatively using the corresponding mathematical model.</p><p><strong>Results: </strong>The diagnostic performance of the network was evaluated using sensitivity, specificity and F1 score, respectively. In the validation set, the automated diagnostic system achieved 0.98 sensitivity, 0.94 specificity, and 0.96 F1 score. In the test set, the system achieved 0.93 sensitivity, 0.79 specificity, and 0.87 F1 score. In quantitative vascular morphology analysis, compared with the healthy control group, the vascular angle of RB patients was increased, while the vascular density, fractal dimension, and number of vascular branches were decreased (all P < 0.001).</p><p><strong>Conclusion: </strong>In this study, we developed an artificial intelligence system for automatic identification and diagnosis of RB in ultra-wide field fundus imaging, and were able to automatically and quantitatively analyze the retinal vascular morphological features of patients with RB.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1962785"},"PeriodicalIF":5.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13638580/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149106585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cystatin F as a neuroimmune effector in CNS inflammation and neurodegeneration.","authors":"Kaitlin Murray, Kellie Fernandez, Thomas E Lane","doi":"10.3389/fcell.2026.1959727","DOIUrl":"10.3389/fcell.2026.1959727","url":null,"abstract":"<p><p>Cystatin F (<i>CST7</i>) has emerged as one of the most consistently upregulated genes identified in transcriptomic and spatial profiling studies of the central nervous system (CNS), particularly within activated microglia and other neuroimmune cell populations. Once regarded primarily as a marker of immune activation, accumulating evidence suggests that the encoded protein, cystatin F, may play a more active role in regulating neuroimmune function through its established ability to modulate lysosomal cysteine proteases. This review synthesizes current knowledge of cystatin F biology and examines its growing relevance across aging, neurodegenerative disease, and CNS inflammation. We first summarize the molecular biology of cystatin F, including its unique intracellular processing, activation, and regulation of cathepsin activity. We then discuss evidence supporting <i>CST7</i> as a conserved marker of activated neuroimmune cells across diverse immune populations and disease-associated cellular states. Next, we review findings implicating <i>CST7</i> across neurodegenerative diseases, highlighting remarkable consistency across distinct pathological contexts. Finally, we examine potential mechanisms linking cystatin F to lysosomal homeostasis, antigen presentation, inflammatory signaling, and cell death pathways. Although direct functional studies within the CNS remain limited, the convergence of biochemical, immunological, and transcriptomic evidence suggests that cystatin F is well positioned to influence neuroimmune responses rather than merely reflect them. Defining the precise role of cystatin F in CNS immunity may therefore provide new insight into the regulation of neuroinflammation and identify novel opportunities for therapeutic intervention across a broad spectrum of neurological diseases.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1959727"},"PeriodicalIF":5.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149106578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aromatic amine exposure and bladder cancer: a review of recent advances in epidemiology, pathogenesis, and prevention.","authors":"Shuxin Li, Yueqiu Zhang, Tie Mao, Jiaqi Wei, Wenyao Zhang, Jingqi Zhang, Wei Wei","doi":"10.3389/fcell.2026.1914792","DOIUrl":"10.3389/fcell.2026.1914792","url":null,"abstract":"<p><p>Aromatic amines are environmental and occupational pollutants found in industrial chemicals, tobacco smoke, hair dyes, and azo-dye-containing textiles. Epidemiological studies confirm that occupational settings and tobacco smoking are the primary sources of exposure, with inhalation and dermal absorption being the major routes of entry, significantly increasing bladder cancer risk. Mechanistically, aromatic amines undergo metabolic activation, leading to DNA adduct formation, oxidative stress, DNA double-strand breaks, and activation of oncogenic signaling pathways such as MAPK/AP-1. Genetic polymorphisms in metabolic enzymes modify individual susceptibility, and risk prediction models incorporating these markers show promise. However, controversies remain regarding low-dose combined exposures, differences in carcinogenic potency among aromatic amines, and inadequate control for confounders in epidemiological studies. Future research should use multi-omics technologies to elucidate complete molecular networks and establish integrated prevention strategies.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1914792"},"PeriodicalIF":5.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13638499/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149106068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}