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Computational Systems Biology Approaches to Cellular Aging - Integrating Network Maps and Dynamical Models. 细胞老化的计算系统生物学方法-整合网络地图和动态模型。
IF 0.6 4区 生物学
Quantitative Biology Pub Date : 2025-12-01 Epub Date: 2025-05-26 DOI: 10.1002/qub2.70007
Hetian Su, Nan Hao
{"title":"Computational Systems Biology Approaches to Cellular Aging - Integrating Network Maps and Dynamical Models.","authors":"Hetian Su, Nan Hao","doi":"10.1002/qub2.70007","DOIUrl":"10.1002/qub2.70007","url":null,"abstract":"<p><p>Cellular aging is a multifaceted, complex process. Many genes and factors have been identified that regulate cellular aging. However, how these genes and factors interact with one another and how these interactions drive the aging processes in single cells remain largely unclear. Recently, computational systems biology has demonstrated its potential to empower aging research by providing quantitative descriptions and explanations of complex aging phenotypes, mechanistic insights into the emergent dynamic properties of regulatory networks, and testable predictions that can guide the design of new experiments and interventional strategies. In general, current complex systems approaches can be categorized into two types: (1) network maps that depict the topologies of large-scale molecular networks without detailed characterization of the dynamics of individual components and (2) dynamical models that describe the temporal behavior in a particular set of interacting factors. In this review, we discuss examples that showcase the application of these approaches to cellular aging, with a specific focus on the progress in quantifying and modeling the replicative aging of budding yeast <i>Saccharomyces cerevisiae</i>. We further propose potential strategies for integrating network maps and dynamical models toward a more comprehensive, mechanistic, and predictive understanding of cellular aging. Finally, we outline directions and questions in aging research where systems-level approaches may be especially powerful.</p>","PeriodicalId":45660,"journal":{"name":"Quantitative Biology","volume":"13 4","pages":""},"PeriodicalIF":0.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12277577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144691910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Nhe1 is required for directional sensing in vegetative Dictyostelium cell migration. Nhe1是营养盘形骨细胞迁移过程中定向传感所必需的。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-06-03 DOI: 10.1080/19336918.2025.2514374
Uri Han, Nara Han, Taeck Joong Jeon
{"title":"Nhe1 is required for directional sensing in vegetative <i>Dictyostelium</i> cell migration.","authors":"Uri Han, Nara Han, Taeck Joong Jeon","doi":"10.1080/19336918.2025.2514374","DOIUrl":"10.1080/19336918.2025.2514374","url":null,"abstract":"<p><p>Na+/H+ exchanger 1 (Nhe1) is a crucial regulator of pH homeostasis and the present study demonstrates that Nhe1 is required for directional sensing in vegetative <i>Dictyostelium</i> cell migration. <i>nhe1</i> null cells exhibited severe defects in directional sensing and migration in response to folate gradients and applied electric fields.Specifically, <i>nhe1</i> null cells failed to exhibit proper translocation of phosphatidylinositol (3,4,5)-trisphosphate (PIP3) to the cell cortex and showed abnormal intracellular calcium signaling upon folate stimulation. Additionally, cells lacking Nhe1 exhibited a reduced capacity to engulf bacteria and latex beads. In contrast, <i>nhe1</i> null cells in the developed stage displayed a defect in cAMP-directed chemotaxis, but normal translocation kinetics of PIP3 to the cell cortex upon cAMP stimulation.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2514374"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215029","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}
引用次数: 0
ACSF2-PGK1 interaction promotes ferroptosis in renal tubular epithelial cells of diabetic nephropathy by regulating Keap1/Nrf2 signaling. ACSF2-PGK1相互作用通过调节Keap1/Nrf2信号通路促进糖尿病肾病肾小管上皮细胞铁下垂。
IF 5.2 2区 生物学
Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-16 DOI: 10.1080/13510002.2025.2529618
Xinran Liu, Chaoyi Chen, Sai Zhu, Xiaomei Luo, Li Gao, Ziyun Hu, Yu Ma, Ling Jiang, Yonggui Wu
{"title":"ACSF2-PGK1 interaction promotes ferroptosis in renal tubular epithelial cells of diabetic nephropathy by regulating Keap1/Nrf2 signaling.","authors":"Xinran Liu, Chaoyi Chen, Sai Zhu, Xiaomei Luo, Li Gao, Ziyun Hu, Yu Ma, Ling Jiang, Yonggui Wu","doi":"10.1080/13510002.2025.2529618","DOIUrl":"10.1080/13510002.2025.2529618","url":null,"abstract":"<p><strong>Objectives: </strong>Recent studies have highlighted the strong association between kidney disease and ferroptosis. However, the role of ferroptosis in diabetic nephropathy (DN) remains unclear. This study aimed to determine the role of ACSF2 in renal tubule injury in DN and its underlying mechanisms.</p><p><strong>Methods: </strong>We established diabetic kidney disease models both in vivo, using db/db mice, and in vitro, using high glucose induced HK-2 cells.</p><p><strong>Results: </strong>A significant upregulation of ACSF2 was observed in the renal tubules of patients with DN and db/db mice. ACSF2 expression correlated with renal tubule injury and renal function, indicating its potential as an independent biomarker in patients with DN. Silencing ACSF2 alleviated high glucose-induced renal tubular epithelial cell injury by reducing oxidative stress-induced ferroptosis in vivo and in vitro. Mechanistically, liquid chromatography-tandem mass spectrometry and co-immunoprecipitation demonstrated that ACSF2 specifically binds to PGK1. ACSF2 affected Keap1 dimerization by regulating PGK1 phosphorylation at serine 203, which subsequently affects the levels of NRF2. Moreover, PGK1 stabilizes ACSF2 via deubiquitination, establishing a positive feedback loop. The results provide evidence that the interaction between ACSF2 and PGK1 promotes DN progression by regulating oxidative stress-induced ferroptosis.</p><p><strong>Discussion: </strong>ACSF2 participates in crosstalk between oxidative stress and ferroptosis. This could be a potential therapeutic target for DN.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2529618"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144650221","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}
引用次数: 0
CpG island demethylation and recruitment of SP1 to the promoter region regulates human thymic stromal lymphopoietin expression. CpG岛去甲基化和SP1在启动子区域的募集调节人胸腺基质淋巴生成素的表达。
IF 2.9 3区 生物学
Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-07-14 DOI: 10.1080/15592294.2025.2529358
Krishna Priya Ganti, Milan Surjit
{"title":"CpG island demethylation and recruitment of SP1 to the promoter region regulates human thymic stromal lymphopoietin expression.","authors":"Krishna Priya Ganti, Milan Surjit","doi":"10.1080/15592294.2025.2529358","DOIUrl":"10.1080/15592294.2025.2529358","url":null,"abstract":"<p><p>Thymic Stromal Lymphopoietin (TSLP), an immunomodulatory cytokine, plays a pivotal role in the development and progression of atopic and allergic diseases. Atopy follows familial inheritance, and genome-wide studies have shown association of atopy with TSLP polymorphisms. Here, we analysed the conserved transcriptional regulatory elements in the human TSLP promoter, which revealed the presence of three CpG islands. Demethylation of the CpG island using 5-azacytidine or siRNA-mediated knockdown of DNA methyl transferases significantly upregulated TSLP expression. Sequence analysis revealed the presence of two overlapping SP1 transcription factor DNA-binding sites (DBSs), between -1494 and -1510 nucleotides on the human TSLP promoter. Further experiments showed that demethylation of the CpG island enables the binding of SP1 to its cognate DBS present on the TSLP promoter, resulting in its transcriptional activation. Moreover, retinoic acid-induced transcription of human TSLP was associated with CpG island demethylation and SP1 binding to the TSLP promoter. These findings unravel a distinct mechanism of transcriptional regulation of the human TSLP gene and suggest possible epigenetic regulation of TSLP expression in modulating atopic and allergic disease severity in different individuals.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2529358"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625618","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}
引用次数: 0
GrimAge and GrimAge2 Age Acceleration effectively predict mortality risk: a retrospective cohort study. 年龄加速有效预测死亡风险:一项回顾性队列研究。
IF 2.9 3区 生物学
Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-07-14 DOI: 10.1080/15592294.2025.2530618
Tieshi Zhu, Yong He, Yixi Wang, Le Zhao
{"title":"GrimAge and GrimAge2 Age Acceleration effectively predict mortality risk: a retrospective cohort study.","authors":"Tieshi Zhu, Yong He, Yixi Wang, Le Zhao","doi":"10.1080/15592294.2025.2530618","DOIUrl":"10.1080/15592294.2025.2530618","url":null,"abstract":"<p><p>Epigenetic clocks have been widely applied to assess biological ageing, with Age Acceleration (AA) serving as a key metric linked to adverse health outcomes, including mortality. However, the comparative predictive value of AAs derived from different epigenetic clocks for mortality risk has not been systematically evaluated. In this retrospective cohort study based on 1,942 NHANES participants (median age 65 years; 944 women), we examined the associations between AAs from multiple epigenetic clocks and the risks of all-cause, cancer-specific, and cardiac mortality. Restricted cubic spline models were used to assess the shape of these associations, and Cox proportional hazards regression was employed to quantify risk estimates. Model performance was compared using the Akaike Information Criterion (AIC) and concordance index (C-index). Our findings revealed that only GrimAge AA and GrimAge2 AA demonstrated approximately linear and positive associations with all three mortality outcomes. Both were significantly associated with increased risks of death, and these associations were consistent across most subgroups. GrimAge and GrimAge2 AAs showed very similar performance in predicting all-cause, cancer and cardiac mortality, with only small differences in AIC values and C-index scores. These findings suggest that both GrimAge and GrimAge2 are effective epigenetic biomarkers for mortality risk prediction and may be valuable tools in future ageing-related research.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2530618"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625619","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}
引用次数: 0
Isopropyl paraben targets type III secretion to inhibit Salmonella enterica serovar typhimurium infection. 对羟基苯甲酸异丙酯靶向III型分泌抑制肠沙门氏菌血清型鼠伤寒杆菌感染。
IF 5.4 1区 农林科学
Virulence Pub Date : 2025-12-01 Epub Date: 2025-08-26 DOI: 10.1080/21505594.2025.2548621
Jinli Ge, Xueyu Li, Qian Lu, Siqi Li, Jiayang Liu, Xuming Deng, Hongtao Liu, Jiazhang Qiu
{"title":"Isopropyl paraben targets type III secretion to inhibit <i>Salmonella enterica</i> serovar typhimurium infection.","authors":"Jinli Ge, Xueyu Li, Qian Lu, Siqi Li, Jiayang Liu, Xuming Deng, Hongtao Liu, Jiazhang Qiu","doi":"10.1080/21505594.2025.2548621","DOIUrl":"10.1080/21505594.2025.2548621","url":null,"abstract":"<p><p><i>Salmonella enterica</i>, a food- and water-borne pathogen, triggers food poisoning and enteric infections. The effectiveness of antibiotics against <i>Salmonella</i> infections is decreasing due to bacterial resistance. Developing novel antimicrobial agents is crucial and urgent. Here, we screened 550 natural compounds and found that isopropyl paraben (IPPB) effectively inhibited <i>Salmonella enterica</i> serovar Typhimurium (ST) invasion of host cells without impacting bacterial growth, reducing the risk of developing bacterial resistance. Further investigation revealed that IPPB bound to the regulatory protein HilD and inhibited the transcription of the type III protein secretion system 1 (T3SS-1) regulatory genes <i>hilD</i>, <i>hilC</i> and <i>rtsA</i>. This interference blocked the production of T3SS-1 effectors. Importantly, IPPB exerted certain therapeutic effects on both <i>G. mellonella</i> larvae and murine models infected with ST and improved the ST-induced gut microbiota dysbiosis in mice. These findings suggest that IPPB has potential as a novel antimicrobial agent, targeting the T3SS-1 of <i>Salmonella</i>.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":" ","pages":"2548621"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12382468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144875460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of Isaria cateniannulata on the colonization process and enzyme activity of Fagopyrum tataricum seeds during germination. 钩藤对苦荞种子萌发定殖过程及酶活性的影响。
IF 5.4 1区 农林科学
Virulence Pub Date : 2025-12-01 Epub Date: 2025-08-15 DOI: 10.1080/21505594.2025.2543062
Xiaona Zhang, Lingdi Gu, Guimin Yang, Can Liu, Kaifeng Huang, Qingfu Chen
{"title":"Effects of <i>Isaria cateniannulata</i> on the colonization process and enzyme activity of <i>Fagopyrum tataricum</i> seeds during germination.","authors":"Xiaona Zhang, Lingdi Gu, Guimin Yang, Can Liu, Kaifeng Huang, Qingfu Chen","doi":"10.1080/21505594.2025.2543062","DOIUrl":"10.1080/21505594.2025.2543062","url":null,"abstract":"<p><p>Endophytic colonization of entomopathogenic fungi has garnered significant attention for its role in promoting plant growth. Specifically, <i>Isaria cateniannulata</i> has shown a positive effect on the germination of <i>Fagopyrum tataricum</i> (buckwheat) seeds, but the mechanisms underlying this promotion remain unclear. This study aims to elucidate the colonization process of <i>I. cateniannulata</i> in <i>F. tataricum</i> seeds during germination stages, quantify the colonization efficiency and tissue specificity of the fungus, and investigate the temporal dynamics of antioxidant enzyme activities and malondialdehyde content triggered by fungal colonization. Furthermore, we evaluated the potential of <i>I. cateniannulata</i>-colonized seedlings to suppress <i>T. urticae</i> populations through oviposition inhibition. The results demonstrated for the first time that <i>I. cateniannulata</i> could successfully colonize germinating <i>F. tataricum</i> seeds during the seed imbibition and germination stages, either by forming dissolution zones with its spores or by germinating and forming mycelia. Initial colonization of all tissues was observed within 16 h, with colonization rates peaking after 5 d, with a preferential colonization rate observed as endosperm > embryo > seed coat. Furthermore, the colonization by <i>I. cateniannulata</i> enhanced peroxidase (POD) activity in the embryo and reduced malondialdehyde (MDA) content. Seedlings grown after colonization were also found to effectively reduce the number of eggs laid by <i>T. urticae</i>. These findings provide both theoretical insights and practical foundations for developing a symbiotic system between <i>I. cateniannulata</i> and <i>F. tataricum</i> seeds.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":" ","pages":"2543062"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12360201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144776305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
ASIC1a Promotes nucleus pulposus derived stem cells apoptosis through modulation of SIRT3-dependent mitochondrial redox homeostasis in intervertebral disc degeneration. ASIC1a通过调节椎间盘退变中sirt3依赖的线粒体氧化还原稳态,促进髓核来源的干细胞凋亡。
IF 5.2 2区 生物学
Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-08 DOI: 10.1080/13510002.2025.2504120
Zhi-Gang Zhang, Liang Kang, Lu-Ping Zhou, Yan-Xin Wang, Chong-Yu Jia, Chen-Hao Zhao, Bo Zhang, Jia-Qi Wang, Hua-Qing Zhang, Ren-Jie Zhang, Cai-Liang Shen
{"title":"ASIC1a Promotes nucleus pulposus derived stem cells apoptosis through modulation of SIRT3-dependent mitochondrial redox homeostasis in intervertebral disc degeneration.","authors":"Zhi-Gang Zhang, Liang Kang, Lu-Ping Zhou, Yan-Xin Wang, Chong-Yu Jia, Chen-Hao Zhao, Bo Zhang, Jia-Qi Wang, Hua-Qing Zhang, Ren-Jie Zhang, Cai-Liang Shen","doi":"10.1080/13510002.2025.2504120","DOIUrl":"10.1080/13510002.2025.2504120","url":null,"abstract":"<p><p>The death of human nucleus pulposus derived stem cells (NPSCs) is a key factor affecting the endogenous repair capability and degeneration of intervertebral discs (IVD). ASIC1a is thought to be closely associated with cells destiny in IVD degeneration (IVDD). However, its physiological and pathological roles in human NPSCs are unclear. In this study, we found that the content of ASIC1a increased with IVDD in both rats and human discs. In acidosis-treated NPSCs, the expression level of ASIC1a increased, accompanied by inhibition of cells viability and activation of mitochondrial apoptotic pathway. Additionally, ASIC1a overexpression activated the mitochondrial apoptotic pathway and increased the level of cellular and mitochondrial ROS in human NPSCs. Moreover, we demonstrated that the dysfunction of SIRT3-regulated mitochondrial redox homeostasis was involved in ASIC1a overexpression-induced apoptosis in human NPSCs. The <i>in vivo</i> experiments also demonstrated that the ASIC1a/SIRT3 pathway was involved in IVDD. Overall, these findings showed that ASIC1a disrupted mitochondrial function and aggravated mitochondrial oxidative stress by inhibiting the expression of SIRT3, which activated human NPSC apoptosis and aggravated IVDD. These findings provide new insights for the development of innovative treatment strategies for IVDD.HighlightsAcidosis inhibited human NPSCs activity and promoted apoptosis via mitochondria.ASIC1a promoted acidosis-induced apoptosis of human NPSCs.ASIC1a inhibited SIRT3 expression, aggravating mitochondrial oxidative stress.ASIC1a promoted IVDD via mitochondrial oxidative stress and apoptosis.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2504120"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584690","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}
引用次数: 0
Identification of fecal microbes as potential biomarkers for early diagnosis of fatty liver disease in cattle. 鉴定粪便微生物作为早期诊断牛脂肪肝的潜在生物标志物。
IF 5.4 1区 农林科学
Virulence Pub Date : 2025-12-01 Epub Date: 2025-07-09 DOI: 10.1080/21505594.2025.2530166
Haoming Sun, Tingjun Liu, Xuyang Song, Sadiq M S Shah, Qin Zhang, Kerong Shi
{"title":"Identification of fecal microbes as potential biomarkers for early diagnosis of fatty liver disease in cattle.","authors":"Haoming Sun, Tingjun Liu, Xuyang Song, Sadiq M S Shah, Qin Zhang, Kerong Shi","doi":"10.1080/21505594.2025.2530166","DOIUrl":"10.1080/21505594.2025.2530166","url":null,"abstract":"<p><p>Fatty liver disease is prevalent during parturition in dairy cattle. Therefore, there is an urgent need to develop novel, sensitive biomarkers for the early diagnosis of the metabolic disorders. Macroproteomics revealed that the faecal microbial community changes significantly when animal develops fatty liver disease. The microbial changes in cows with severe fatty liver (SFL) were greater than cows with moderate fatty liver (MFL) and normal condition (Norm). This suggests that microorganisms play an important role in the pathogenesis of metabolic disorders. In this study, faeces-sourced microorganisms and microbial proteins were identified and testified as novel biomarkers for the early diagnosis of fatty liver disease in cattle. For example, the AUC (area under curve) values, based on Receiver Operating Characteristics analysis, of using the combination of <i>Lachnoanaerobaculum</i> and <i>Bifidobacterium</i> (at the <i>genus</i> level) to discriminate MFL and SFL animals reached 0.944 and 0.867, respectively, and 0.922 and 0.985, respectively, for the combination of <i>Bifidobacterium pseudolongum</i> and <i>Lachnospiraceae bacterium</i> (at the <i>species</i> level). Interestingly, the differentially expressed microbial proteins are closely related to the identified microorganisms. For example, the majority of the top 20 microbial proteins with significant expression differences were derived from <i>Bifidobacterium pseudolongum</i>. <i>Bifidobacterium pseudolongum</i> was considered a prominent potential biomarker for the diagnosis of metabolic disorders, especially in fatty liver cattle. The results of this study confirm that faecal microbial dysbiosis signatures can serve as a diagnosis biomarker for non-alcoholic fatty liver disease (NAFLD), but also shed light on faecal microbiota transfer (FMT) experiments in treating NAFLD.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2530166"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247111/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144601676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A comprehension and systematic insight into the interaction between ferroptosis and virus infection: The implications of mechanisms and strategies. 对铁下垂和病毒感染之间相互作用的理解和系统见解:机制和策略的含义。
IF 5.4 1区 农林科学
Virulence Pub Date : 2025-12-01 Epub Date: 2025-07-14 DOI: 10.1080/21505594.2025.2532806
Sai Niu, Yian Deng, Yonggen Yang, Junjie Wang, Chunyue Fang, Ying Zhou, Hanchuan Dai
{"title":"A comprehension and systematic insight into the interaction between ferroptosis and virus infection: The implications of mechanisms and strategies.","authors":"Sai Niu, Yian Deng, Yonggen Yang, Junjie Wang, Chunyue Fang, Ying Zhou, Hanchuan Dai","doi":"10.1080/21505594.2025.2532806","DOIUrl":"10.1080/21505594.2025.2532806","url":null,"abstract":"<p><p>Ferroptosis is a novel form of iron-dependent programmed cell death characterized by iron metabolic derangement, an abnormal antioxidant system, and lipid peroxidation. Emerging evidence revealed that viruses modulate ferroptosis to facilitate their replication, dissemination, and pathogenesis, thereby promoting infection or achieving immune evasion by hijacking the host's iron metabolism. However, the interplay between ferroptosis and virus infections remains to be elucidated. This review comprehensively summarizes the core mechanisms of ferroptosis, including iron homeostasis, the system Xc<sup>-</sup>/GPX4 pathway, the FSP1/CoQ10 pathway, lipid peroxidation, and their essential roles were discussed in ferroptosis. We highlighted the relationship between the core mechanisms of ferroptosis and virus infection. Furthermore, we revealed the underlying pathogenic mechanisms of viral infections and the prospective applications targeting ferroptosis. This article is conducive to deepening our understanding of the regulatory mechanism of ferroptosis, unraveling the potential therapeutic intervention and pharmacological direction for the development of innovative ferroptosis-dependent antiviral agents.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2532806"},"PeriodicalIF":5.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269692/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144627268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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