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Dual-Direction of DNA Methylome Reprogramming During Rice Domestication 认领 引用
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作者 YU Xiaoman CHENG Xiang +8 位作者 LI Yilin YU Ruoqian LIU Jiajia YANG Lingwei HE Huiying WEI Hua SHANG Lianguang WANG Yuexing LIU Xiangpei 《Rice science》 SCIE CAS CSCD 2026年第3期287-291,I0153-I0170,共5页
Crop domestication has been attributed predominantly to selection on DNA sequence variation,yet the role of epigenetic factors remains largely unknown.Here,we conducted a genome-wide comparative methylome analysis of ... Crop domestication has been attributed predominantly to selection on DNA sequence variation,yet the role of epigenetic factors remains largely unknown.Here,we conducted a genome-wide comparative methylome analysis of African and Asian wild and cultivated rice species,revealing extensive methylation reprogramming during domestication. 展开更多
关键词 methylomeanalysis crop domestication dual direction methylome reprogramming rice domestication epigenetic factors genomewide sequencevariation methylation reprogramming comparative epigenetic factors
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Steroid hormone ouabain cooperates with Na+,K+-ATPase to improve innate immunity against bacterial infections through a non-classic training mechanism regulated by mRNA reprogramming 认领 引用
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作者 Lili Chen Kuida Chen +8 位作者 RunRun Shan Jinjun Bian PeiPei Jin Hao Lin Jian Liu Yan Chen Siyao Zhu Fangzhou Yin Wu Yin 《Acta Pharmaceutica Sinica B》 SCIE CAS CSCD 2026年第6期3655-3679,共25页
Epigenetic reprogramming underpins trained immunity(TRIM).However,the importance of mRNA reprogramming in TRIM remains unknown.Here,we discovered,for the first time,that the steroid hormone ouabain creates a significa... Epigenetic reprogramming underpins trained immunity(TRIM).However,the importance of mRNA reprogramming in TRIM remains unknown.Here,we discovered,for the first time,that the steroid hormone ouabain creates a significant training effect on peripheral innate immune cells(IICs),leading to functional enhancement of IICs against bacterial infections.However,unlike conventional training mechanisms,ouabain primarily relies on an integrated posttranscriptional RNA regulon complex(IPRRC)to establish immune memory and reprogram cytokine expression,with lncRNA-CYTOR playing a critical role in this process.Moreover,to enhance training effects while reducing lactate production,ouabain promotes a rapid degradation of the Na+,K+-ATPase receptor.Pathologically,endogenous ouabain is downregulated in sepsis-induced immunoparalysis in vivo,correlating with impaired innate immunity.Exogenous ouabain rescue significantly reverses this impairment,and its effect is superior to β-glucan,even when used at one percent of β-glucan dosage.Notably,posttranscriptional RNA regulons are also critically involved in β-glucan’s training effects.Overall,mRNA reprogramming emerges as a new mechanism for TRIM;steroid hormone ouabain is a novel innate immunity regulator. 展开更多
关键词 Innate immune cells Immune training mRNA reprogramming Endotoxin tolerance Posttranscriptional RNA regulons Steroid hormone ouabain Na+,K+-ATPase CYTOR
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Pristimerin ameliorates spasmolytic polypeptide-expressing metaplasia by modulating Cdkn1c(p57)-mediated glycolytic reprogramming 认领 引用
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作者 Jun-Song Wen Zi-Wei Pan +2 位作者 Xue-Dan Yao Yan-Qing Liu Yao-Dong Zhu 《World Journal of Gastroenterology》 SCIE CAS 2026年第10期94-115,共22页
BACKGROUND Spasmolytic polypeptide-expressing metaplasia(SPEM)is a gastric precancerous lesion(GPL)with high malignant potential.The ethyl acetate extract of Celastrus orbiculatus Thunb.effectively ameliorates GPL and... BACKGROUND Spasmolytic polypeptide-expressing metaplasia(SPEM)is a gastric precancerous lesion(GPL)with high malignant potential.The ethyl acetate extract of Celastrus orbiculatus Thunb.effectively ameliorates GPL and gastric cancer progression.Meanwhile,the primary active constituent of this plant,pristimerin,also demonstrates notable antitumor activity.AIM To investigate the therapeutic effects of pristimerin on SPEM and its underlying mechanisms.METHODS Pristimerin was administered to high-dose tamoxifen-induced SPEM mice to assess its effects on pathological progression,glycolytic reprogramming,and Cdkn1c(p57)expression.Human gastric epithelial(GES-1)cells were treated with tamoxifen and then with pristimerin or 2-deoxy-D-glucose to demonstrate that pristimerin ameliorates SPEM by regulating glycolytic reprogramming.Furthermore,gastric organoids were treated with N-methyl-N’-nitro-N-nitrosoguanidine/Helicobacter pylori,followed by Cdkn1c overexpression or knockdown and then pristimerin,to confirm p57 as the key target through which pristimerin regulates glycolytic reprogramming and reverses SPEM.RESULTS Pristimerin effectively ameliorated gastric mucosal damage and oxyntic atrophy induced by high-dose tamoxifen,suppressed the aberrant upregulation of key glycolytic regulators,SPEM-specific markers,and stem cell markers,and upregulated p57 expression.In tamoxifen-induced GES-1 cells,pristimerin exhibited comparable therapeutic effects.Crucially,glycolysis inhibition in GES-1 cells effectively ameliorated tamoxifen-induced SPEM-associated phenotypes.In gastric organoids,Cdkn1c overexpression suppressed glycolytic reprogramming and SPEM phenotype activation,whereas Cdkn1c knockdown attenuated pristimerin-mediated inhibition of glycolysis and amelioration of SPEM.CONCLUSION Pristimerin effectively ameliorates gastric mucosal pathological damage and oxyntic atrophy in high-dose tamoxifen-induced SPEM mice,and improves SPEM progression by modulating Cdkn1c(p57)-mediated glycolytic reprogramming. 展开更多
关键词 Pristimerin Spasmolytic polypeptide-expressing metaplasia Glycolytic reprogramming Cdkn1c Gastric organoids Gastric precancerous lesion
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Immunometabolic Reprogramming in Hepatocellular Carcinoma Mechanisms,Biomarkers,and Therapeutic Implications 认领 引用
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作者 Guodong Yu Weiying Ge +6 位作者 Hongliang Yao Xuefeng Bai Jianfei Wu Yuan Wang Jiangtao Bai Yong Cui Jijing Han 《Oncology Research》 SCIE 2026年第7期321-356,共36页
Hepatocellular carcinoma(HCC)develops in a chronically inflamed and dysregulated liver metabolism,in which tumor progression and resistance to treatment are orchestrated by the changes in cellular metabolism and immun... Hepatocellular carcinoma(HCC)develops in a chronically inflamed and dysregulated liver metabolism,in which tumor progression and resistance to treatment are orchestrated by the changes in cellular metabolism and immune control.Growing evidence recognizes immunometabolic reprogramming as the two-way interaction of metabolic processes and immune cell capabilities as one of the major determinants of immune evasion and heterogeneity of treatment response in HCC.The review aims to comprehensively evaluate immunometabolic reprogramming in hepatocellular carcinoma,with a focus on its role in tumor progression,immune regulation,and its potential for biomarker identification and therapeutic targeting.Dysregulated glycolysis,lipid metabolism,amino acid utilization,and mitochondrial dysfunction contribute to remodeling of the tumor microenvironment and defects in antitumor immunity.Immunometabolic biomarkers derived from tumor tissue,immune cell states,circulating and liquid biopsy platforms,and metabolic imaging are critically examined for their clinical relevance and associations with disease outcomes and treatment responses.Besides,the role of different immunometabolic conditions on therapeutic efficacy,specifically within the frames of immune checkpoint-inhibitor-based and combination regimens,is addressed.Altogether,immunometabolic reprogramming is identified as a common framework of biomarker-based stratification and precision therapeutic techniques in hepatocellular carcinoma. 展开更多
关键词 Metabolic reprogramming tumor microenvironment biomarkers immune checkpoint hepatocellular carcinoma
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Circular RNAs:Key Regulators of Tumor Metabolic Reprogramming and Clinical Translation 认领 引用
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作者 Yimao Wu Yitong Liu +4 位作者 Ruowei Sun Yiyuan Zhang Qian Zhang Chen Li Mengyao Li 《Oncology Research》 SCIE 2026年第3期1-37,共37页
Tumor metabolic reprogramming is a core hallmark of cancer,characterized by pathways such as aerobic glycolysis,aberrant lipid metabolism,and glutaminolysis that support rapid proliferation and immunosuppressive micro... Tumor metabolic reprogramming is a core hallmark of cancer,characterized by pathways such as aerobic glycolysis,aberrant lipid metabolism,and glutaminolysis that support rapid proliferation and immunosuppressive microenvironments.Circular RNAs(circRNAs)are highly stable,evolutionarily conserved non-coding RNAs that have emerged as critical modulators of these metabolic shifts.This review aims to systematically elucidate the roles and mechanisms of circRNAs in reprogramming tumor metabolism,and to discuss their clinical potential as biomarkers and therapeutic targets.Through mechanisms including miRNA sponging,protein interactions,regulation of mitochondrial dynamics,and modulation of metabolic enzymes,circRNAs influence key metabolic pathways by targeting glycolytic enzymes,lipid synthesis regulators,and glutaminolysis-related molecules to either facilitate or inhibit their expression.This review systematically summarizes the unique contributions of circRNAs to tumor metabolic reprogramming,highlighting key mechanisms such as regulation of peptide-encoding protein translation,mitochondrial localization function,gene promoter-targeted transcriptional regulation,and cross-pathway metabolic mediation,which underscore their distinct biological advantages and regulatory roles in tumor metabolism.The stability and tissue specificity of circRNAs make them promising diagnostic biomarkers,while their role in drug resistance mediated by metabolic reprogramming highlights their potential as therapeutic targets.Strategies such as circRNA inhibitors,mimics,and nanoparticle-based delivery systems are being explored to modulate tumor metabolism.Despite challenges including complex regulatory networks and limited manipulation tools,advances in high-throughput technologies and clinical trials hold promise for translating circRNA research into novel cancer therapies. 展开更多
关键词 Biomarkers circRNAs glutaminolysis lipid metabolism metabolic reprogramming therapeutic targets tumor metabolism
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Navigating the Metabolic-Genomic Paradigm:Mitochondrial Reprogramming as a Driver of Cancer Plasticity 认领 引用
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作者 Yen-Dun Tony Tzeng Chen-Yueh Wen +3 位作者 Su-Boon Yong Zhi-Hong Wen An-Jen Chiang Chia-Jung Li 《Oncology Research》 SCIE 2026年第8期102-123,共22页
Breast cancer(BC)management has transitioned from histological classification to molecular subtyping,yet therapeutic resistance and intratumor heterogeneity remain critical clinical challenges.This review examines the... Breast cancer(BC)management has transitioned from histological classification to molecular subtyping,yet therapeutic resistance and intratumor heterogeneity remain critical clinical challenges.This review examines the emerging paradigm shift toward integrating mitochondrial metabolism into the precision medicine framework.We detail the complex mitonuclear crosstalk where nuclear genetic alterations,such as Breast Cancer 1(BRCA1)deficiency and TP53 mutations,fundamentally reprogram mitochondrial bioenergetics.Specifically,the loss of BRCA1 function triggers a systemic NAD+depletion trap through PARP1 hyperactivation,while oncogenic drivers like MYC coordinate with PGC1?to enhance mitochondrial biogenesis for metastatic survival.We evaluate the diagnostic potential of mitochondrial DNA heteroplasmy and machine learning derived metabolic gene signatures as high performance biomarkers for patient stratification and the detection of minimal residual disease via liquid biopsy.Furthermore,we analyze current clinical efforts to target mitochondrial vulnerabilities,including respiratory chain inhibitors like metformin and BH3 mimetics,while highlighting the significant challenges posed by metabolic plasticity and nutrient competition in the tumor microenvironment.The analysis of clinical trial data,such as the MA.32 study,suggests that metabolic interventions require precise patient selection based on specific metabolic phenotypes rather than broad application.Looking forward,the integration of genome scale metabolic models and artificial intelligence(AI)offers a transformative pathway to simulate patient specific metabolic fluxes and identify novel synthetic lethal targets.By bridging the gap between nuclear genomic drivers and dynamic mitochondrial adaptations,this review aims to provide a preliminary framework for the exploration of metabolic-genomic precision oncology in BC. 展开更多
关键词 Breast cancer(BC) precision medicine metabolic reprogramming therapeutic resistance artificial intelligence(AI)
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Cold exposure induces transcriptomic and metabolic reprogramming in the heart:An integrated multi-omics study 认领 引用
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作者 Jiaming Ju Zhengchao Wen +6 位作者 Jiayun Li Dandan Zhang Kejiao Zhang Haozhan Wang Roman E.Tokmachev Yang Li Yanan Jiang 《Frigid Zone Medicine》 2026年第2期97-108,I0067-I0118,共12页
Objective:Exposure to extreme cold temperatures may increase the risk of cardiovascular diseases.This study aimed to investigate the effects of cold exposure on the heart and its underlying mechanisms using an integra... Objective:Exposure to extreme cold temperatures may increase the risk of cardiovascular diseases.This study aimed to investigate the effects of cold exposure on the heart and its underlying mechanisms using an integrated transcriptomic and metabolomic approach.Methods:C57BL/6 mice were subjected to cold exposure at 4°C for 12 hours per day for 4 weeks.Transcriptomics and metabolomics profiles of the heart were analyzed.Differentially expressed genes(DEGs)and differentially expressed metabolites(DEMs)were identified,and mRNA expression levels were validated by qRT-PCR.Enrichment analyses were performed to identify significantly affected pathways.Transcriptomic and metabolomic data were then integrated to provide a comprehensive view of molecular alterations induced by cold exposure.To further evaluate the relationship between cold exposure and cardiovascular diseases,a myocardial infarction(MI)mouse model was established,and overlapping genes between cold exposure and MI were analyzed.Results:Cold exposure significantly altered both the transcriptomic and metabolomic profiles of mouse hearts.Pathway enrichment analyses based on DEGs and DEMs identified several signaling pathways affected by cold stress.Integrated transcriptomic and metabolomic analyses further highlighted potential metabolic and signaling pathways associated with cold exposure.By cross-referencing DEGs associated with cold exposure with those from the MI model in the GEO database(GSE223208),34 overlapping genes were identified.Integrated analyses implicated key genes(Tnfrsf12a and Nppb)in cold-aggravated cardiac remodeling,which were further validated in MI models.Conclusion:Cold exposure reprograms the cardiac transcriptome and metabolome in mice.Cold exposure and MI share a subset of DEGs,which may help illuminate the pathophysiological interplay between cold stress and MI,highlighting potential therapeutic targets for cold-exacerbated cardiovascular diseases. 展开更多
关键词 integrated omics transcriptomic reprogramming metabolomic reprogramming cardiovascular diseases gene expression metabolomics profiles integrated transcriptomic metabolomic approachmethods c bl cold exposure
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Lactate metabolism and epigenetic reprogramming drive c-KIT hyperactivation to mediate Gilteritinib resistance:Rationale for c-KIT degraders over kinase inhibitors 认领 引用
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作者 Yanli Zhao Yubo Wang +8 位作者 Ning Liu Yijie Yang Jialu Li Ziqi Huang Lan Ma Shuang Yang Shuangwei Liu Jingfeng Zhou Guang Yang 《Acta Pharmaceutica Sinica B》 SCIE CAS CSCD 2026年第6期3764-3783,共20页
Kinase inhibitors targeting FLT3-ITD,such as Gilteritinib,have emerged as promising targeted therapies.However,recent clinical trials have shown disappointing overall survival(OS)outcomes in acute myeloid leukemia(AML... Kinase inhibitors targeting FLT3-ITD,such as Gilteritinib,have emerged as promising targeted therapies.However,recent clinical trials have shown disappointing overall survival(OS)outcomes in acute myeloid leukemia(AML)patients,primarily due to disease recurrence following treatment.We uncovered a potential mechanism underlying Gilteritinib resistance.Gilteritinib treatment induced reprogramming of lactic acid metabolism in AML cells,leading to increased H3K27 lactylation that continuously amplified c-KIT expression and signaling in AML cells.This mechanism enriched leukemia stem cells(LSCs),driving drug resistance and disease relapse.Notably,c-KIT kinase inhibitors failed to effectively counteract the progression of relapsed and refractory AML,as c-KIT overexpression results in amplification of its signaling.To address this issue,a dual degrader targeting both FLT3-ITD and c-KIT was identified.Beyond exhibiting stronger efficacy than Gilteritinib in inhibiting AML cell proliferation,this PROTAC also demonstrates a significant ability to induce cell differentiation.In cell line-derived xenograft(CDX)models,the degrader significantly suppressed FLT3-ITD+AML recurrence and prolonged the survival of experimental mice.Furthermore,in PDX model established using AML cells from Gilteritinib-resistant patients,the degrader showed significantly superior therapeutic efficacy compared to the combination treatment of Gilteritinib and Imatinib.As a candidate drug molecule,this degrader exhibits promising potential for clinical translation. 展开更多
关键词 FLT3-ITD Gilteritinib Drug resistance c-KIT Targeted protein degradation Lactate metabolism reprogramming PDX
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Reprogramming of amino acid metabolism in cholangiocarcinoma:A potential target for metabolic-targeted therapy 认领 引用
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作者 Kullanat Khawkhiaw Worachart Lert-Itthiporn +2 位作者 Naisana Seyedasli Ching-Feng Chiu Charupong Saengboonmee 《World Journal of Gastroenterology》 SCIE CAS 2026年第13期8-26,共19页
The incidence of cholangiocarcinoma(CCA),a highly aggressive malignancy of the bile duct epithelia,has been gradually increasing worldwide.However,curative treatments are still limited.Novel therapeutic strategies are... The incidence of cholangiocarcinoma(CCA),a highly aggressive malignancy of the bile duct epithelia,has been gradually increasing worldwide.However,curative treatments are still limited.Novel therapeutic strategies are urgently needed to improve patients’survival and quality of life.Metabolic reprogramming has been well recognized as one of the hallmark processes supporting the development of several cancer types,including CCA.Apart from the Warburg effect and high glucose requirement in CCA cells,amino acid metabolism is also found to be essential in CCA development and progression.Upregulation of proteins and enzymes involved in amino acid metabolism is reported in CCA,typically associated with a poor prognosis for patients.Targeting these proteins and enzymes has been shown to retard CCA progression,and thus,they are promising targets for drug development.This article reviews the reprogramming of amino acid metabolism in CCA and its roles in CCA progression,such as aggressive phenotypes.The up-to-date development of therapeutic agents targeting particular proteins in amino acid metabolism is also discussed.A summary of the current knowledge gap and directions for further research are also provided and proposed. 展开更多
关键词 Amino acid Biliary tract cancer Cancer metabolism Cholangiocarcinoma Metabolic reprogramming
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Metabolic reprogramming of microglia:Effects on development,disease,and therapeutic potential 认领 引用
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作者 Haiwei Zhang Mengmeng Jin +1 位作者 Peng Jiang Ying Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第10期4633-4641,共9页
Microglia,the immune sentinels of the central nervous system,play vital roles in maintaining neural homeostasis and mediating responses to injury and disease.Their functions,including synaptic pruning to neuroinflamma... Microglia,the immune sentinels of the central nervous system,play vital roles in maintaining neural homeostasis and mediating responses to injury and disease.Their functions,including synaptic pruning to neuroinflammation,are tightly linked to their metabolic state.Emerging evidence suggests that metabolic reprogramming is a key driver of microglial activation,functional transitions,and interactions with neurons and other glial cells.This review summarizes current findings on the developmental origins,region-specific adaptations,and metabolic plasticity of microglia.We review lipid metabolism,energy utilization,and oxidative stress responses,which underlie immune regulation and neuroprotective functions.By integrating molecular,transcriptomic,and metabolomic insights,we provide a comprehensive understanding of microglial metabolism and highlight potential therapeutic strategies targeting metabolic pathways in neurodegenerative and central nervous system diseases. 展开更多
关键词 energy metabolism functional states human induced pluripotent stem cells lipid metabolism metabolic reprogramming microglia neurodegenerative disease neuroinflammation
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Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer 认领 引用
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作者 Xiaomeng Li Xuejiao Li +1 位作者 Hongbo Wu Rui Li 《Oncology Research》 SCIE 2026年第4期302-330,共29页
Lung cancer remains the leading cause of cancer-related mortality worldwide,primarily driven by metabolic reprogramming and immune evasion mechanisms within tumor cells.To adapt to the nutrient-deprived tumor microenv... Lung cancer remains the leading cause of cancer-related mortality worldwide,primarily driven by metabolic reprogramming and immune evasion mechanisms within tumor cells.To adapt to the nutrient-deprived tumor microenvironment(TME),lung cancer cells undergo profound metabolic reprogramming,characterized by enhanced glycolysis(the Warburg effect),increased glutamine dependency(mediated by GLS1),and accelerated lipid synthesis(involving enzymes such as FASN).These metabolic alterations not only remodel the TME but also dampen antitumor immune responses by promoting immunosuppressive cell populations(e.g.,Tregs and M2 macrophages)and inhibiting effector functions of CD8+T cells and natural killer(NK)cells.Critically,a bidirectional crosstalk operates between tumor cell metabolism and the immunosuppressive TME:metabolic reprogramming drives immune suppression through metabolite accumulation,whereas the immunosuppressive TME,in turn,promotes tumor cell adaptability—thus forming a positive feedback loop that reinforces immune evasion and therapy resistance.This review elucidates key molecular pathways governing metabolic reprogramming in lung cancer—spanning glucose,amino acid,and lipid metabolism—and their dynamic crosstalk with immune regulation,including epigenetic modifications and non-coding RNA-mediated mechanisms.Additionally,it evaluates emerging therapeutic strategies targeting the metabolic-immune axis,such as inhibitors of HK2 or GLS1 combined with anti-PD-1/PD-L1 agents,which aim to reverse immunosuppression and improve clinical outcomes.By synthesizing recent advances,this work provides a theoretical framework for precision oncology interventions,highlighting the potential of metabolic immunotherapies and future directions integrating AI and multi-omics data to overcome resistance in lung cancer. 展开更多
关键词 Lung cancer metabolic reprogramming immune evasion tumor microenvironment metabolicimmune axis
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Branched-Chain Amino Acid Metabolic Reprogramming and Cancer:Molecular Mechanisms,Immune Regulation,and Precision Targeting 认领 引用
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作者 Dongchi Cai Jialin Ji +1 位作者 Chunhui Yang Hong Cai 《Oncology Research》 SCIE 2026年第1期174-201,共28页
Metabolic reprogramming involving branched-chain amino acids(BCAAs)—leucine,isoleucine,and valine—is increasingly recognized as pivotal in cancer progression,metastasis,and immune modulation.This review comprehensiv... Metabolic reprogramming involving branched-chain amino acids(BCAAs)—leucine,isoleucine,and valine—is increasingly recognized as pivotal in cancer progression,metastasis,and immune modulation.This review comprehensively explores how cancer cells rewire BCAA metabolism to enhance proliferation,survival,and therapy resistance.Tumors manipulate BCAA uptake and catabolism via high expression of transporters like L-type amino acid transporter 1(LAT1)and enzymes including branched chain amino acid transaminase 1(BCAT1),branched chain amino acid transaminase 2(BCAT2),branched-chain alpha-keto acid dehydrogenase(BCKDH),and branched chain alpha-keto acid dehydrogenase kinase(BCKDK).These alterations sustain energy production,biosynthesis,redox homeostasis,and oncogenic signaling(especially mammalian target of rapamycin complex 1[mTORC1]).Crucially,tumor-driven BCAA depletion also shapes an immunosuppressive microenvironment,impairing anti-tumor immunity by limiting essential nutrients for T cells and natural killer(NK)cells.Innovative therapeutic strategies targeting BCAA pathways—ranging from selective small-molecule inhibitors(e.g.,LAT1 and BCAT1/2)to dietary modulation—have shown promising preclinical and early clinical efficacy,highlighting their potential to exploit metabolic vulnerabilities in cancer cells while bolstering immune responses.By integrating multi-omics data and precision targeting approaches,this review underscores the translational significance of BCAA metabolic reprogramming,positioning it as a novel frontier in cancer treatment. 展开更多
关键词 Branched-chain amino acids metabolic reprogramming tumor microenvironment targeted therapy
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Post-translational modifications in hepatocellular carcinoma:Linking senescence,metabolic reprogramming,and immune evasion for therapeutic innovation 认领 引用
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作者 Tai-Xian Song Yao Rong +1 位作者 Hao-Min Ji Xing-Sheng Wang 《World Journal of Gastrointestinal Oncology》 SCIE 2026年第6期35-60,共26页
Hepatocellular carcinoma remains a leading cause of cancer mortality.Although immune checkpoint inhibitors have improved outcomes for a subset of patients,primary and acquired resistance are common.Post-translational ... Hepatocellular carcinoma remains a leading cause of cancer mortality.Although immune checkpoint inhibitors have improved outcomes for a subset of patients,primary and acquired resistance are common.Post-translational modifications(PTMs)provide a rapid and reversible regulatory layer that links oncogenic signaling,metabolism,and chromatin state to cellular senescence and the tumor microenvironment.Here we synthesize evidence showing how ubiquitination,phosphorylation,acetylation,methylation,SUMOylation,O-GlcNAcylation,and lactylation modulate core senescence programs(p53etinoblastoma protein,DNA-damage response)and the senescence-associated secretory phenotype,thereby shaping myeloid recruitment,T-cell dysfunction,and immune evasion in hepatocellular carcinoma.We further discuss how metabolism-coupled PTMs rewire glycolysis-epigenetics crosstalk and generate spatially confined senescence-metabolic-immune niches that can be resolved by single-cell and spatial multi-omics.The current evidence base is dominated by mechanistic studies and correlative clinical datasets,underscoring the need for prospective validation and standardized PTM/senescence biomarkers.Finally,we propose a sequential“induce-remodel-clear”therapeutic concept in which senescence induction is paired with PTM-targeted modulation and immune or senolytic clearance to improve response durability. 展开更多
关键词 Hepatocellular carcinoma Post-translational modifications Cellular senescence Tumor immune microenvironment Metabolic reprogramming Immunotherapy Single-cell multi-omics Spatial transcriptomics Therapy resistance Precision medicine
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Genetic redirection of morphogenic signaling for induced cell fate reprogramming 认领 引用
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作者 Soon Hyung Bae Pil Joon Seo 《Journal of Integrative Plant Biology》 SCIE CAS CSCD 2026年第6期1597-1600,共4页
Plants have long been recognized for their remarkableability to reprogram differentiated somatic cells into new cell types,organs,or even entire plants(Chen et al.,2024).This property has been extensively exploited th... Plants have long been recognized for their remarkableability to reprogram differentiated somatic cells into new cell types,organs,or even entire plants(Chen et al.,2024).This property has been extensively exploited through in vitro tissue culture,which has become a foundational tool for plant propagation and genetic engineering in the genome engineering era.In tissue culture,explants from plant organs,such as leaves,hypocotyls,or roots,are de-differentiated into a rapidly proliferating,undifferentiated cell mass called callus,which can subsequently regenerate into whole plants.The success of tissue culture relies largely on the precise balance of phytohormones in the culture medium,particularly auxins(e.g.,2,4-D,NAA,and IAA)and cytokinins(e.g.,BAP,kinetin,and zeatin)(Chen et al.,2024). 展开更多
关键词 vitro tissue culturewhich cell fate reprogramming tissue cultureexplants differentiated somatic cells plants genetic engineering genome engineering genetic redirection
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Monocyte reprogramming and trained immunity:Linking metabolism to inflammation in non-alcoholic fatty liver disease 认领 引用
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作者 Stanislav Kotlyarov 《World Journal of Hepatology》 2026年第4期84-90,共7页
Non-alcoholic fatty liver disease(NAFLD)represents a global clinical challenge,largely due to the liver’s central role as a key immunometabolic organ.Recent research underscores the systemic immunometabolic nature of... Non-alcoholic fatty liver disease(NAFLD)represents a global clinical challenge,largely due to the liver’s central role as a key immunometabolic organ.Recent research underscores the systemic immunometabolic nature of NAFLD.It has been shown that peripheral blood immune cells of NAFLD patients exist in a primed state,which aligns with the concept of long-term functional reprogramming of innate immune cells in metabolic diseases.This functional reprogramming-encompassing priming and trained immunity-represents a recently described facet of innate immunity.While evolutionarily beneficial for host defense,these mechanisms are now recognized as contributors to the pathogenesis of various chronic non-communicable diseases.It is hypothesized that monocyte reprogramming,induced by chronic exposure to metabolic signals such as lipotoxicity and hyperglycemia,fosters a hyperactive pro-inflammatory phenotype.This phenotype significantly contributes to disease pathogenesis and the development of systemic immunometabolic disturbances.Understanding the role of immunometabolic reprogramming opens new prospects for the search of biomarkers and the development of therapeutic strategies aimed at modulating the metabolism of immune cells in NAFLD. 展开更多
关键词 Non-alcoholic fatty liver disease Innate immune system Immunometabolism Metabolic reprogramming Priming Trained immunity Monocytes
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Endothelial metabolic reprogramming influences tumor immune microenvironment 认领 引用
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作者 Ming Chen Zhi-Gang Chen 《World Journal of Clinical Oncology》 2026年第3期29-44,共16页
The components of the tumor microenvironment are crucial in tumor growth,metastasis,immune evasion and therapeutic resistance.To adapt to the lowoxygen and nutrient-deficient conditions,cancer cells generate new blood... The components of the tumor microenvironment are crucial in tumor growth,metastasis,immune evasion and therapeutic resistance.To adapt to the lowoxygen and nutrient-deficient conditions,cancer cells generate new blood vessels to promote tumor expansion and metastatic spread via tumor angiogenesis.Recent research has revealed that tumor endothelial cells reprogram their metabolic patterns during tumor progression.These metabolic changes influence the infiltration of cytotoxic T lymphocytes such as CD8+T cells and recruit immunesuppressive cells,resulting in immune evasion and increased tumor progression.Therefore,targeting tumor endothelial metabolism alongside immunotherapies could offer a novel strategy for precise cancer treatment in clinical settings. 展开更多
关键词 Tumor microenvironment Tumor endothelial cells Metabolic reprogramming Immunosuppression Immunotherapy
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Platelet-derived mitochondria transfer accelerates fracture healing by promoting osteogenic differentiation and metabolic reprogramming of adipose-derived stem cells 认领 引用
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作者 Zhu Pan Rui Zhang +3 位作者 Gai-Mei Du Ji-Hai Yi Jin Bao Cai-Dong Liu 《World Journal of Stem Cells》 SCIE 2026年第7期167-184,共18页
BACKGROUND Platelets promote fracture repair by transferring mitochondria to recipient cells.Adipose-derived stem cells(ASCs)have garnered significant attention in bone regeneration due to their osteogenic differentia... BACKGROUND Platelets promote fracture repair by transferring mitochondria to recipient cells.Adipose-derived stem cells(ASCs)have garnered significant attention in bone regeneration due to their osteogenic differentiation potential.AIM To investigate the effect of platelet-derived mitochondria on ASC osteogenesis and elucidate the underlying molecular mechanism.METHODS ASCs were isolated from Sprague-Dawley rats and characterized.ASCs were treated with platelets isolated from rat whole blood or platelet-derived mitochondria,and then evaluated for glycolysis and osteogenic differentiation.Histone lactylation and its impact on gene transcription were analyzed.A rat closed femoral fracture model was established to evaluate mitochondrial roles in vivo.RESULTS Platelets enhanced glycolysis and osteogenic differentiation of ASCs.Platelet-derived mitochondria exhibit a similar pro-osteogenic and metabolic effect,and these mitochondria were found to be internalized by ASCs.Mitochondria induced H3K18 lactylation,which enriched the promoters of AXIN2,BMPR1B,COL1A1,and OSTN,thereby promoting their transcription.2-deoxy-D-glucose treatment or H3K18R transfection reversed the mitochondrial-induced enhancement of glycolysis and osteogenesis.Additionally,platelet-derived mitochondria amplified ASC-mediated fracture repair,an effect counteracted by 2-deoxy-D-glucose.CONCLUSION Platelet-derived mitochondrial transfer promotes osteogenic gene transcription via H3K18 lactylation,facilitating osteogenic differentiation and accelerating fracture healing.This study reveals a novel metabolic-epigenetic mechanism in fracture repair. 展开更多
关键词 Adipose-derived stem cells Platelet-derived mitochondria Osteogenic differentiation Glycolysis Histone lactylation Fracture healing Metabolic reprogramming Epigenetic regulation
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Grapevine cell response to carbon deficiency requires transcriptome and methylome reprogramming 认领 引用 被引量：1
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作者 Margot M.J.Berger Virginie Garcia +9 位作者 Nathalie Lacrampe Bernadette Rubio Guillaume Decros Pierre Pétriacq Amélie Flandin Cédric Cassan Ghislaine Hilbert-Masson Sophie Colombié Rossitza Atanassova Philippe Gallusci 《Horticulture Research》 SCIE CSCD 2025年第1期129-142,共14页
Sugar limitation has dramatic consequences on plant cells,which include cell metabolism and transcriptional reprogramming,and the recycling of cellular components to maintain fundamental cell functions.There is howeve... Sugar limitation has dramatic consequences on plant cells,which include cell metabolism and transcriptional reprogramming,and the recycling of cellular components to maintain fundamental cell functions.There is however no description of the contribution of epigenetic regulations to the adaptation of plant cells to limited carbon availability.We investigated this question using nonphotosynthetic grapevine cells(Vitis vinifera,cv Cabernet Sauvignon)cultured in vitro with contrasted glucose concentrations.Sugar depletion in the culture medium led to a rapid cell growth arrest and a major metabolic shift that include the depletion in soluble sugar and total amino acids and modulation of the cell redox status.Consistently,flux modeling showed a dramatic slowdown of many pathways required for biomass accumulation such as cell wall and protein synthesis.Sugar depletion also resulted in a major transcriptional reprogramming,characterized by the induction of genes involved in photosynthesis,and the repression of those related to sucrose mobilization or cell cycle control.Similarly,the epigenetic landscape was deeply modified.Glucose-depleted cells showed a higher global DNA methylation level than those grown with glucose.Changes in DNA methylation mainly occurred at transposable elements,and at genes including some of those differentially expressed,consistent with an important role for methylation to the adaptation of cells to limited sugar availability.In addition,genes encoding histone modifiers were differentially expressed suggesting that additional epigenetic mechanisms may be at work in plant cells under carbon shortage. 展开更多
关键词 epigenetic regulations plant cells carbon deficiency transcriptome reprogramming sugar limitation cell metabolism recycling cellular components transcriptional reprogrammingand
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Reprogramming to restore youthful epigenetics of senescent nucleus pulposus cells for mitigating intervertebral disc degeneration and alleviating low back pain 认领 引用 被引量：4
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作者 Wenzheng Ma Wantao Wang +9 位作者 Lei Zhao Jinghao Fan Lei Liu Lin Huang Baogan Peng Jianru Wang Baoshan Xu Hongmei Liu Decheng Wu Zhaomin Zheng 《Bone Research》 SCIE CAS CSCD 2025年第3期716-730,共15页
Aging is a pivotal risk factor for intervertebral disc degeneration(IVDD)and chronic low back pain(LBP).The restoration of aging nucleus pulposus cells(NPCs)to a youthful epigenetic state is crucial for IVDD treatment... Aging is a pivotal risk factor for intervertebral disc degeneration(IVDD)and chronic low back pain(LBP).The restoration of aging nucleus pulposus cells(NPCs)to a youthful epigenetic state is crucial for IVDD treatment,but remains a formidable challenge.Here,we proposed a strategy to partially reprogram and reinstate youthful epigenetics of senescent NPCs by delivering a plasmid carrier that expressed pluripotency-associated genes(Oct4,Klf4 and Sox2)in Cavin2-modified exosomes(OKS@M-Exo)for treatment of IVDD and alleviating LBP.The functional OKS@M-Exo efficaciously alleviated senescence markers(p16INK4a,p21CIP1and p53),reduced DNA damage and H4K20me3 expression,as well as restored proliferation ability and metabolic balance in senescent NPCs,as validated through in vitro experiments.In a rat model of IVDD,OKS@M-Exo maintained intervertebral disc height,nucleus pulposus hydration and tissue structure,effectively ameliorated IVDD via decreasing the senescence markers.Additionally,OKS@MExo reduced nociceptive behavior and downregulated nociception markers,indicating its efficiency in alleviating LBP.The transcriptome sequencing analysis also demonstrated that OKS@M-Exo could decrease the expression of age-related pathways and restore cell proliferation.Collectively,reprogramming by the OKS@M-Exo to restore youthful epigenetics of senescent NPCs may hold promise as a therapeutic platform to treat IVDD. 展开更多
关键词 youthful epigenetics senescent nucleus pulposus cells intervertebral disc degeneration reprogramming intervertebral disc degeneration ivdd low back pain nucleus pulposus cells npcs partially reprogram reinstate youthful epigenetics
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Metabolic reprogramming: a new option for the treatment of spinal cord injury 认领 引用 被引量：2
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作者 Jiangjie Chen Jinyang Chen +11 位作者 Chao Yu Kaishun Xia Biao Yang Ronghao Wang Yi Li Kesi Shi Yuang Zhang Haibin Xu Xuesong Zhang Jingkai Wang Qixin Chen Chengzhen Liang 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第4期1042-1057,共16页
Spinal cord injuries impose a notably economic burden on society,mainly because of the severe after-effects they cause.Despite the ongoing development of various therapies for spinal cord injuries,their effectiveness ... Spinal cord injuries impose a notably economic burden on society,mainly because of the severe after-effects they cause.Despite the ongoing development of various therapies for spinal cord injuries,their effectiveness remains unsatisfactory.However,a deeper understanding of metabolism has opened up a new therapeutic opportunity in the form of metabolic reprogramming.In this review,we explore the metabolic changes that occur during spinal cord injuries,their consequences,and the therapeutic tools available for metabolic reprogramming.Normal spinal cord metabolism is characterized by independent cellular metabolism and intercellular metabolic coupling.However,spinal cord injury results in metabolic disorders that include disturbances in glucose metabolism,lipid metabolism,and mitochondrial dysfunction.These metabolic disturbances lead to corresponding pathological changes,including the failure of axonal regeneration,the accumulation of scarring,and the activation of microglia.To rescue spinal cord injury at the metabolic level,potential metabolic reprogramming approaches have emerged,including replenishing metabolic substrates,reconstituting metabolic couplings,and targeting mitochondrial therapies to alter cell fate.The available evidence suggests that metabolic reprogramming holds great promise as a next-generation approach for the treatment of spinal cord injury.To further advance the metabolic treatment of the spinal cord injury,future efforts should focus on a deeper understanding of neurometabolism,the development of more advanced metabolomics technologies,and the design of highly effective metabolic interventions. 展开更多
关键词 axons glycolysis metabolic reprogramming metabolism mitochondria neural regeneration neuroprotection oxidative phosphorylation spinal cord injury therapy
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