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Long-term aerobic exercise enhances circulating exosomal miR-214-3p to promote endothelial progenitor cell-mediated repair of endothelial damage induced by obesity 认领 引用 被引量：2
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作者 Junhao Huang Peilun Li +6 位作者 Bing Shen Huiwen Gao Shen Wang Pingyu Wang Weiji Deng Dongdong Gao Min Hu 《Journal of Sport and Health Science》 SCIE CAS CSCD 2026年第6期80-95,共16页
Background Exercise training may counteract the detrimental effects of obesity on endothelial function by enhancing the reparative capabilities of endothelial progenitor cells(EPC);however,the underlying mechanisms of... Background Exercise training may counteract the detrimental effects of obesity on endothelial function by enhancing the reparative capabilities of endothelial progenitor cells(EPC);however,the underlying mechanisms of exercise-induced EPC-mediated endothelial repair are still unclear.The present study aimed to determine the mechanisms by which exercise-induced circulating exosomes protect against endothelial dysfunction induced by obesity.Methods An 8-week aerobic exercise intervention in both obese human participants and high-fat diet-induced obese rats was conducted.Circulating exosomes were isolated and characterized.microRNA sequencing,molecular biology techniques,and functional assays(including proliferation,migration,and luciferase reporter assays)were employed to identify key exosomal microRNAs and their downstream targets.A microRNA-214-3p(miR-214-3p)knockout rat model was used to validate its role in vivo.Results Exercise promoted EPC-mediated repair of endothelial damage and upregulated exosomal miR-214-3p in both obese humans and rats,without altering exosome quantity.miR-214-3p enhanced EPC proliferation and migration directly,by upregulating collagen type I alpha 2 chain(COL1A2)expression,and indirectly,through the phosphatase and tensin homolog,phosphatidylinositol 3-kinase,serinehreonine kinase(PTEN-PI3K-Akt)signaling pathway.Knockout of miR-214-3p abolished the exercise-induced improvements in endothelial and EPC functionalities.The myocardium was identified as an important source of the exercise-induced increase in circulating exosomal miR-214-3p.Conclusion Long-term aerobic exercise promotes endothelial repair in obesity by enriching circulating exosomes with miR-214-3p,which enhances EPC function via the PTEN-PI3K-Akt pathway and direct regulation of COL1A2.These findings reveal a novel exosome-mediated mechanism through which exercise improves vascular health and suggest potential therapeutic strategies for obesity-related endothelial dysfunction. 展开更多
关键词 Obesity Exercise Endothelial cells Endothelial progenitor cells Exosomes
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Insights into the transcriptomic heterogeneity of brain endothelial cells in normal aging and Alzheimer’s disease 认领 引用 被引量：1
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作者 Qian Yue Shang Li +3 位作者 Chon Lok Lei Huaibin Wan Zaijun Zhang Maggie Pui Man Hoi 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第2期569-576,共8页
Drug development for Alzheimer’s disease is extremely challenging,as demonstrated by the repeated failures of amyloid-β-targeted therapeutics and the controversies surrounding the amyloid-βcascade hypothesis.More r... Drug development for Alzheimer’s disease is extremely challenging,as demonstrated by the repeated failures of amyloid-β-targeted therapeutics and the controversies surrounding the amyloid-βcascade hypothesis.More recently,advances in the development of Lecanemab,an anti-amyloid-βmonoclonal antibody,have shown positive results in reducing brain A burden and slowing cognitive decline in patients with early-stage Alzheimer’s disease in the Phase Ⅲ clinical trial(Clarity Alzheimer’s disease).Despite these promising results,side effects such as amyloid-related imaging abnormalities(ARIA)may limit its usage.ARIA can manifest as ARIA-E(cerebral edema or effusions)and ARIA-H(microhemorrhages or superficial siderosis)and is thought to be caused by increased vascular permeability due to inflammatory responses,leading to leakages of blood products and protein-rich fluid into brain parenchyma.Endothelial dysfunction is an early pathological feature of Alzheimer’s disease,and the blood-brain barrier becomes increasingly leaky as the disease progresses.In addition,APOE4,the strongest genetic risk factor for Alzheimer’s disease,is associated with higher vascular amyloid burden,increased ARIA incidence,and accelerated blood-brain barrier disruptions.These interconnected vascular abnormalities highlight the importance of vascular contributions to the pathophysiology of Alzheimer’s disease.Here,we will closely examine recent research evaluating the heterogeneity of brain endothelial cells in the microvasculature of different brain regions and their relationships with Alzheimer’s disease progression. 展开更多
关键词 Alzheimer’s disease brain microvessel endothelial cells transcriptomic heterogeneity endothelial activation blood-brain barrier impairment neurovascular cell-cell communication
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Prognostic significance of vascular endothelial dysfunction in patients with vasospastic angina 认领 引用 被引量：1
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作者 Hiroki Teragawa Yu Hashimoto +1 位作者 Akane Tsuchiya Shuichi Nomura 《World Journal of Cardiology》 2026年第3期67-77,共11页
BACKGROUND Vascular endothelial dysfunction(VED)is thought to contribute to the pathogenesis of vasospastic angina(VSA),but its prognostic significance remains unclear.AIM To evaluate whether clinical characteristics ... BACKGROUND Vascular endothelial dysfunction(VED)is thought to contribute to the pathogenesis of vasospastic angina(VSA),but its prognostic significance remains unclear.AIM To evaluate whether clinical characteristics and prognosis differ according to the presence or absence of VED in patients with VSA.METHODS We retrospectively analyzed 244 patients(mean age 67 years,107 men)admitted for chest pain screening and diagnosed with VSA by spasm provocation testing.Vascular endothelial function was evaluated using brachial artery flow-mediated dilation(FMD).Patients were divided into a high-FMD group(≥3.7%;n=123)and a low-FMD group(FMD-L,<3.7%;n=121).VSA was defined as≥90%coronary vasoconstriction on angiography with chest symptoms and/or electrocardiographic changes during spasm provocation testing.Focal spasm was defined as spasm localized within a single American Heart Association coronary segment.Major adverse cardiovascular events included cardiac death and cardiovascular rehospitalization.RESULTS Baseline characteristics,except for age(P=0.017),did not differ significantly between groups.Focal spasm tended to be more frequent in the FMD-L group(43%vs 32%,P=0.069).Kaplan-Meier analysis showed a significantly lower major adverse cardiovascular events-free survival rate in the FMD-L group(log-rank P=0.004).Multivariate Cox regression identified FMD-L(P=0.025)and older age(P=0.026)as independent prognostic factors,whereas focal spasm was not significant(P=0.157).CONCLUSION VED is an independent predictor of adverse outcomes in VSA.Evaluation of endothelial function may provide valuable prognostic information in patients with VSA. 展开更多
关键词 Coronary spasm Endothelial function Flow-mediated dilation Focal spasm Vasospastic angina Vascular endothelial dysfunction
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Abnormalities of liver sinusoidal endothelial cells in primary biliary cholangitis 认领 引用
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作者 Evangelos Thalassinos George Notas +4 位作者 Costantinos Xidakis Ioannis Drygiannakis Ourania Sfakianaki Ioannis Tsomidis Elias Kouroumalis 《World Journal of Experimental Medicine》 2026年第1期219-231,共13页
BACKGROUND Liver sinusoidal endothelial cells(LSECs)may have a critical role in the pathogenesis of primary biliary cholangitis(PBC)that has not been investigated.AIM To investigate the role of LSECs in PBC.METHODS We... BACKGROUND Liver sinusoidal endothelial cells(LSECs)may have a critical role in the pathogenesis of primary biliary cholangitis(PBC)that has not been investigated.AIM To investigate the role of LSECs in PBC.METHODS We studied the levels of soluble vascular cell adhesion molecule-1,soluble intercellular adhesion molecule-1 and soluble E-selectin and the tissue plasminogen activator(t-PA)and its inhibitor in the serum of 30 PBC patients before and 25 patients after treatment with ursodeoxycholic acid(UDCA).Moreover,immortalized endothelial cells(EA.hy926)were incubated with serum from patients with PBC,hepatitis C virus(HCV)and normal controls for up to 24 hours.The expression of endothelin(ET)1,ET2,ET3,and ET receptors A and B were also measured by quantitative polymerase chain reaction.RESULTS Vascular cell adhesion molecule and intercellular adhesion molecule were significantly increased in PBC and HCV with the highest values found in PBC patients.UDCA had no effect.Levels were significantly higher in late PBC(stages III-IV),compared with early PBC(stages I-II).t-PA was significantly increased in PBC but not in HCV.Higher values were obtained in late PBC.UDCA decreased t-PA.Plasminogen activator inhibitor-1 levels were similar in all groups.Expression of endothelin 1,endothelin 2,and endothelin 3 significantly varied at different time points.ET receptors A was decreased at 2 hours and 6 hours in PBC,and at 2 hours and 24 hours in HCV.ET receptors B was reduced at 2 hours and 24 hours in both PBC and HCV.CONCLUSION Endothelial adhesion molecules are abnormal in PBC particularly in the late fibrotic stages.ET and their receptors are reduced in LSECs after incubation with PBC and HCV sera,findings that might be related to pathogenesis. 展开更多
关键词 Primary biliary cholangitis Sinusoidal endothelial cells Endothelial markers Endothelins Endothelin receptors
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The HCMV-encoded miR-UL36-3p promotes angiogenesis of endothelial cells by downregulating FOXO3 认领 引用
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作者 Chen Wang Mengyu Li +3 位作者 Guosheng Li Hao Zhang Cheng Wang Chen-Yu Zhang 《Animal Models and Experimental Medicine》 CAS CSCD 2026年第5期980-990,共11页
Background:Human cytomegalovirus(HCMV)infection is related to the acceleration of transplant vascular sclerosis,atherosclerosis,and coronary restenosis.A shared theme of these vascular illnesses is pathologic angiogen... Background:Human cytomegalovirus(HCMV)infection is related to the acceleration of transplant vascular sclerosis,atherosclerosis,and coronary restenosis.A shared theme of these vascular illnesses is pathologic angiogenesis.Nevertheless,how HCMV infection causes angiogenesis is not fully understood.Human serum contains HCMV-encoded miRNAs,and it is unclear whether these virus-derived miRNAs can regulate angiogenesis.This research looks into HCMV-encoded miRNA's role in an-giogenesis of endothelial cells.Methods:Endothelial cell proliferation was examined by CCK8 assay,and cell migra-tion capability was established using a Transwell Boyden Chamber.Western blotting alongside luciferase reporter assay verified the direct regulation of FOXO3 by HCMV-encoded miRNAs,including hcmv-miR-UL36-3p.hcmv-miR-UL36-3p's pro-angiogenic action was examined by angiogenesis assays(in vivo)and capillary tube formation(in vitro),which were performed by giving C57BL/6J mice subcutaneous Matrigel injections containing bFGF along with simultaneous injections of either hcmv-miR-UL36-3p or ncRNA once every 4 days.After 8 days,Matrigel plugs were examined.Results:hcmv-miR-UL36-3p was upregulated in patients with atherosclerosis.Overexpression of hcmv-miR-UL36-3p enhanced capillary tube development,motil-ity,and proliferation in endothelial cells.hcmv-miR-UL36-3p promoted endothelial cell tube formation through directly binding to and downregulating FOXO3.Experiments in mice further confirmed that hcmv-miR-UL36-3p promoted angiogenesis in vivo.Conclusions:The HCMV-encoded miR-UL36-3p can trigger angiogenesis in endothe-lial cells by targeting FOXO3.Our work provides a conceivable mechanism of how HCMV-encoded miRNAs contribute to vascular illness. 展开更多
关键词 angiogenesis atherosclerosis endothelial cell FOXO3 HCMV miRNA
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Endothelial cell injury:a crucial link in microcirculatory dysfunction associated with sepsis 认领 引用
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作者 Yuhui Pan Yanyan Ma +3 位作者 Ke Wan Yizhou Xu Guoxing Wang Miaorong Xie 《World Journal of Emergency Medicine》 SCIE CAS CSCD 2026年第1期28-35,共8页
BACKGROUND:Sepsis is a prevalent and severe condition,with microcirculation disruptions playing a crucial role in its progression.Endothelial cell(EC)injury is the primary factor behind microcirculatory issues.This re... BACKGROUND:Sepsis is a prevalent and severe condition,with microcirculation disruptions playing a crucial role in its progression.Endothelial cell(EC)injury is the primary factor behind microcirculatory issues.This review is to outline the pathomechanism,organ heterogeneity,biomarkers,and therapeutic implications of endothelial dysfunction in sepsis,off ering references and insights for the clinical management of sepsis.METHODS:A systematic search of Web of Science and PubMed from inception to June 10,2025,limited to English publications,was conducted.Two reviewers independently identifi ed studies on EC injury in patients with septic microcirculatory dysfunction.Duplicate articles based on multiple search criteria were excluded.RESULTS:Fifty-nine articles,including cell,animal,and clinical studies,were included.These studies reported the effects of EC injury on the microcirculation in sepsis,including changes in vascular permeability,coagulation dysfunction,vasomotor regulation,and infl ammatory responses.These pathways interact and ultimately lead to septic microcirculation disorders.CONCLUSION:Sepsis-induced endothelial dysfunction involves various interconnected mechanisms,which collectively compromise ECs and impede microcirculatory perfusion.Future research should enhance current understanding of endothelial injury mechanisms,develop synergistic multi-target strategies to disrupt this cycle,and facilitate the clinical application of endothelial markers for early intervention and dynamic assessment. 展开更多
关键词 Sepsis Endothelial cells Vascular permeability Coagulation dysfunction Vasomotor regulation Infl ammatory responses Microcirculatory
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Krill oil activates NRF2 to prevent diabetic endothelial injury in part through astaxanthin-induced inhibition of KEAP1 认领 引用
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作者 Huali Meng Xiaoli Huang +6 位作者 Jian Zhou Yan Zheng Lei Du Hui Li Zhiyue Zhang Linlin Xu Hao Wu 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第3期1069-1083,共15页
Diabetes mellitus(DM)is a severe chronic disease that results in high morbidity and mortality.DM causes endothelial injury(DEI)as a basis for cardiovascular complications of DM with few effective approaches developed ... Diabetes mellitus(DM)is a severe chronic disease that results in high morbidity and mortality.DM causes endothelial injury(DEI)as a basis for cardiovascular complications of DM with few effective approaches developed for its intervention.Krill oil(KO)possesses anti-inflammatory and anti-oxidative activities,but its effect on DEI is unknown.Hence,the aims of this study were to investigate the effect and molecular mechanism of KO on DEI.To investigated the preventive effect of KO on DEI,streptozotocin and high-fat diet-induced type 2 diabetic mice were fed with KO for 6 months.RNA sequencing for endothelial cells(ECs)was used to explore the mechanism of KO's protective function.To clarify the role of nuclear factor erythroid 2-related factor 2(Nfe2l2 or NRF2)signaling in KO's protection against DEI,Nfe2l2 gene-silenced ECs or knockout mice were treated with KO.Molecular docking assay and surface plasmon resonance assay were carried out to reveal binding between Kelch like ECH associated protein 1(KEAP1)and major components of KO.KO significantly alleviated DEI and aortic pathological injury in the wild-type diabetic mice.RNA sequencing revealed that KO dramatically activated NRF2 antioxidant signaling in high glucose-challenged ECs,the effect of which was further confirmed in the diabetic aortas.Nfe2l2 gene deletion or silencing completely abolished KO's protection against DEI in vivo and in vitro,demonstrating that NRF2 was required for KO's action.Further,molecular docking assay and surface plasmon resonance assay identified that KO's functional component astaxanthin(AST),but not docosahexaenoic acid and eicosapentaenoic acid,was able to bind the Kelch domain of KEAP1,promoting nuclear translocation of NRF2 which activated antioxidant gene expression.The comparison of the effects of KO and AST on endothelial NRF2 nuclear translocation suggested that KO might activate NRF2 at least partially through AST-KEAP1 interaction.KO activates NRF2 to prevent diabetic endothelial injury in part through AST-induced inhibition of KEAP1. 展开更多
关键词 Diabetes Endothelial Kelch like ECH associated protein 1 Krill oil Nuclear factor erythroid 2-related factor 2
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ETS1 Regulates Endothelial AQP1 Expression via Interaction withMEF2C in Endothelial Cells 认领 引用
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作者 Yong Jiang Rui Ma +3 位作者 Yu-ge Wu Yi-ming Huo Han-zhu Zhou Jun-xuan Zhang 《BIOCELL》 SCIE 2026年第4期224-236,共13页
Background:Aquaporin 1(AQP1)plays a key role inmyocardial ischemia-reperfusion(I/R)injury.This study aimed to elucidate themechanisms bywhich erythroblast transformation-specific 1(ETS1)andmyocyte enhancer factor 2C(M... Background:Aquaporin 1(AQP1)plays a key role inmyocardial ischemia-reperfusion(I/R)injury.This study aimed to elucidate themechanisms bywhich erythroblast transformation-specific 1(ETS1)andmyocyte enhancer factor 2C(MEF2C)regulated AQP1 transcription.Methods:Human umbilical vein endothelial cells(HUVECs)and rats with coronary heart disease were employed for in vitro and in vivo experiments,respectively.Expressions of ETS1,MEF2C,and AQP1 were analyzed by western blotting and quantitative reverse transcription polymerase chain reaction(qRT-PCR).Chromatin immunoprecipitation(ChIP)and co-immunoprecipitation(Co-IP)assays were performed to confirm the interactions between ETS1 and MEF2C.Scratch wound healing and transwell assays were performed to assess the migration of HUVECs.Tube formation was conducted to assess the angiogenesis of HUVECs.HE and Masson staining were performed to assess the pathological changes and fibrosis of cardiac tissues;Immunofluorescence of platelet endothelial cell adhesion molecule(CD31)and AQP1 was performed to assess vascular endothelial cell dysfunction in cardiac tissues of rats with coronary heart disease.Results:ETS1 overexpression upregulated both MEF2C and AQP1 expressions,while ETS1 silencing induced the opposite results.ETS1 and MEF2C interacted with each other and bound to the proximal promoter of AQP1.MEF2C synergized with ETS1 to promote the migration and tube formation of HUVECs,which were abolished by AQP1 silencing.I/R injury caused structural damage and fibrosis of cardiac tissues in rats,whichwere relieved by ETS1 andMEF2C silencing.Also,the increasedAQP1 andCD31 levels in cardiac tissues of rats induced by I/R injury were reversed by ETS1 andMEF2C knockdown.Conclusion:These results highlight the ETS1/MEF2C/AQP1 pathway as a potential therapeutic target for endothelial and vascular disorders. 展开更多
关键词 Erythroblast transformation specific 1 aquaporin 1 myocyte enhancer factor 2C endothelial cells
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Integrative Analysis of scRNA-Seq and Bulk RNA-Seq Reveals Novel Transcription Factor Regulating Endothelial Heterogeneity Induced by Lrg1 Following Cerebral Ischemia-Reperfusion 认领 引用
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作者 Shaofeng Xiong Wenkai Lv +4 位作者 Guosheng Cao Longsheng Fu Wen Liu Mengfan Lei Yanni Lv 《BIOCELL》 SCIE 2026年第1期248-272,共25页
Objective:Leucine-rich alpha-2 glycoprotein 1(Lrg1)could regulate diverse cells in cerebral ischemiareperfusion.Our study seeks to uncover Lrg1’s impact on endothelial cell heterogeneity via differentiation pathways ... Objective:Leucine-rich alpha-2 glycoprotein 1(Lrg1)could regulate diverse cells in cerebral ischemiareperfusion.Our study seeks to uncover Lrg1’s impact on endothelial cell heterogeneity via differentiation pathways and transcription factors.Method:The CSOmap model measured cell-to-brain-center distances using single-cell RNA sequencing(scRNA-seq)data in middle cerebral artery occlusion reperfusion(MCAO/R).Monocle2 mapped endothelial differentiation paths.Gene set enrichment analysis(GSEA)analyzed endothelial subcluster variations.Database searches revealed a zinc finger MIZ-type containing 1 protein-frizzled 3(Zmiz1-Fzd3)promoter interaction.Endothelial cells were transfected with a Fzd3 promoter-luciferase plasmid.Polymerase chain reaction(PCR)and western blotting assessed MCAO/R or Zmiz1 overexpression effects on Fzd3-related mRNA and proteins.A retroviral vector carrying Zmiz1 was injected into the brains of mice to study its effect on Fzd3.Result:Lrg1−/−mice exhibited elevated cell adhesion proteins and decreased microvascular leakage after MCAO/R.CSOmap showed widened astrocyte spacing in thesemice.RSS revealed Zmiz1 overexpression inMCAO/R+Lrg1−/−mice.MCAO/R and pcDNA3-Zmiz1 transfection both enhanced luciferase activity with Fzd3,indicating Zmiz1 binding to Fzd3.Retroviral Zmiz1 injection or knockdown disrupted ischemic brain tight junctions,highlighting Zmiz1’s key role in blood-brain barrier protection,likely through Fzd3 pathway modulation.Conclusion:The findings indicate Lrg1 knockout induces endothelial differentiation by activating Zmiz1,which is crucial for maintaining blood-brain barrier function,possibly via modulating the Fzd3 pathway. 展开更多
关键词 Single-cell RNA sequencing endothelial heterogeneity leucine-rich alpha-2 glycoprotein 1 zinc finger MIZ-type containing 1 Protein Frizzled 3 transcription factor cerebral ischemia reperfusion
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Rethinking vascular repair:Endothelial ageing,progenitor cell dysfunction,and senotherapeutic rescue 认领 引用
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作者 Ulvi Bayraktutan 《Life Research》 2026年第2期14-21,共8页
Vascular ageing is increasingly recognised as a key driver of cardiovascular and cerebrovascular disease rather than merely a passive consequence of chronological time.Progressive loss of endothelial regenerative capa... Vascular ageing is increasingly recognised as a key driver of cardiovascular and cerebrovascular disease rather than merely a passive consequence of chronological time.Progressive loss of endothelial regenerative capacity remains central to this process and is characterised by endothelial progenitor cell dysfunction,accumulation of senescent endothelial cells,and aberrant changes in the endothelial secretome.Taken together these alterations contribute to ineffective endothelial repair,chronic(low-grade)vascular inflammation and impaired endothelial barrier integrity and function,ultimately leading to vascular dysfunction.Over the past two decades,accumulating evidence from our group and others has provided mechanistic insight into how oxidative stress,redox imbalance,mitochondrial dysfunction and cellular senescence collectively impair endothelial(barrier)function and compromise overall vascular homeostasis.Age-dependent changes in progenitor cell number and function further limit the capacity of vasculature to respond to damage and stress.More recent work demonstrate that senolytics and senomorphics can preserve endothelial function and delay age-related vascular and cerebral barrier dysfunction in experimental models.This mini review supports an emerging framework that positions defective endothelial renewal as a critical driver of vascular ageing and endothelial dysfunction.We propose that concomitant application of senotherapeutics with progenitor cell-based or secretome-based approaches represents a critical next step in precision vascular medicine. 展开更多
关键词 vascular ageing endothelial regeneration endothelial progenitor cells cellular senescence senotherapeutics blood-brain barrier oxidative stress
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Promising biomarkers for mild cognitive impairment and Alzheimer's disease:Levels of soluble endothelial glycocalyx products 认领 引用
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作者 Carmela Rita Balistreri Roberto Monastero 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第10期4892-4893,共2页
A previous study has described a strong relationship between cardio-and cerebrovascular risk factors and the onset and progression of cognitive impairment(CI),and Alzheimer's disease(AD),although their pathophysio... A previous study has described a strong relationship between cardio-and cerebrovascular risk factors and the onset and progression of cognitive impairment(CI),and Alzheimer's disease(AD),although their pathophysiology remains not completely understood(Balistreri,2021). 展开更多
关键词 cognitive impairment soluble products Alzheimers disease alzheimers disease ad cardiovascular risk factors endothelial glycocalyx biomarkers cerebrovascular risk factors
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Endothelial metabolic reprogramming influences tumor immune microenvironment 认领 引用 被引量：1
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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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LECT2/Tie1/Src signaling regulates the oxidative stress response in endothelial cells and liver ischemia-reperfusion injury 认领 引用
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作者 Yu Yang Shi-Li Wu +6 位作者 Zhi-Hao Huang Meng-Qi Dong Zhi-Min Liu Meng Xu Yi Gao Wei-Jie Zhou Yuan Lin 《World Journal of Hepatology》 2026年第6期223-233,共11页
BACKGROUND Hepatic ischemia-reperfusion injury(IRI)is a critical pathological process associated with trauma,sepsis,and liver surgeries,including transplantation.During reperfusion,oxidative stress in sinusoidal endot... BACKGROUND Hepatic ischemia-reperfusion injury(IRI)is a critical pathological process associated with trauma,sepsis,and liver surgeries,including transplantation.During reperfusion,oxidative stress in sinusoidal endothelial cells triggers cell death,however,the underlying regulatory mechanisms remain poorly defined.Previous studies have implicated leukocyte-derived chemotaxin-2(LECT2)in various diseases and identified it as a ligand for the orphan receptor Tie1,yet its role in endothelial cell injury during liver IRI remains unclear.AIM To investigate whether LECT2 exacerbates liver IRI by regulating oxidative stress in endothelial cells through the Tie1/Src signaling pathway and to evaluate the therapeutic potential of targeting this axis.METHODS In vitro hypoxia-reoxygenation injury was modeled in EA.hy926 endothelial cells,followed by LECT2 knockdown or recombinant LECT2 treatment,Tie1 silencing,and Tie1-Ig3 segment protein treatment to block LECT2/Tie1 binding.Src kinase activity was inhibited using dasatinib.Cell viability,oxidative stress,cytotoxicity,and signaling pathway activation were assessed.In vivo,LECT2 knockout mice underwent hepatic ischemiareperfusion,while injury markers,inflammatory cytokines,and endothelial damage were evaluated.RESULTS LECT2 knockdown reduced oxidative stress and endothelial cell damage following hypoxia-reoxygenation,whereas recombinant LECT2 exacerbated these effects.Disruption of LECT2/Tie1 binding,via either Tie1 knockdown or Tie1-Ig3 treatment mitigated injury.Mechanistically,LECT2 activated Src kinase phosphorylation in a Tie1-dependent manner,and Src inhibition reversed LECT2-induced cell damage.In mice,LECT2 deletion attenuated liver IRI,decreased apoptosis and inflammation,and better preserved sinusoidal endothelial integrity.CONCLUSION The LECT2/Tie1/Src signaling axis plays a critical role in regulating oxidative stress and endothelial cell injury during hepatic ischemia-reperfusion.Targeting the LECT2/Tie1/Src signaling pathway may offer a novel therapeutic strategy for mitigating liver IRI in clinical settings. 展开更多
关键词 Leukocyte-derived chemotaxin-2 Tie1 Src kinase Endothelial cells Oxidative stress Ischemia-reperfusion injury Liver injury
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Improving endothelial dysfunction:An important mechanism of traditional Chinese medicine in reducing the occurrence of severe dengue 认领 引用
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作者 Jiao Tang Si-Qi Li +3 位作者 Yuan-Yuan Chen De-Hong Ma Wei-Bo Wen Huan-Tian Cui 《Infectious Diseases Research》 2026年第1期10-12,共3页
Dengue fever is an acute infectious disease caused by the dengue virus and transmitted by mosquito vectors[1].Its clinical manifestations include high fever,headache,muscle and joint pain,and rash.It holds a significa... Dengue fever is an acute infectious disease caused by the dengue virus and transmitted by mosquito vectors[1].Its clinical manifestations include high fever,headache,muscle and joint pain,and rash.It holds a significant position in global public health.In recent years,its incidence has continued to rise worldwide[2],making it one of the major diseases threatening human health.The disease course of dengue fever is divided into three typical phases:the acute febrile phase,the critical phase,and the recovery phase.While most patients experience mild symptoms,some may progress to severe dengue and potentially fatal outcomes if not promptly and effectively treated during the critical phase. 展开更多
关键词 mosquito vectors its dengue fever dengue virus acute infectious disease severe dengue acute febrile endothelial dysfunction traditional chinese medicine
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Significance of flow-mediated dilation in evaluating endothelial dysfunction in vasospastic angina 认领 引用
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作者 Wilbert Huang 《World Journal of Cardiology》 2026年第5期13-17,共5页
A previous retrospective cohort study evaluated flow-mediated dilation(FMD)as a marker of endothelial-dependent vasodilation and nitroglycerin-induced dilation as a marker of endothelial-independent vasodilation in va... A previous retrospective cohort study evaluated flow-mediated dilation(FMD)as a marker of endothelial-dependent vasodilation and nitroglycerin-induced dilation as a marker of endothelial-independent vasodilation in vasospastic angina patients.The study demonstrated that low FMD(<3.7%)was significantly associated with major adverse cardiovascular events,whereas low nitroglycerininduced dilation(<14%)was not.Multivariable Cox proportional hazards modeling was carefully limited to three covariates to avoid overfitting in the setting of a small number of events.Important contributors to endothelial dysfunction,including smoking,chronic kidney disease,and inflammatory status,were acknowledged,and baseline use of endothelial-protective medications did not differ between groups.Despite limitations related to its retrospective design and sample size,the study supports the prognostic value of FMD in vasospastic angina and highlights endothelial dysfunction as a key determinant of adverse outcomes. 展开更多
关键词 Flow-mediated dilation Vasospastic angina Endothelial dysfunction Coronary artery disease Prognosis
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Yang Mai Tong Luo formula ameliorates heart failure with preserved ejection fraction by alleviating microvascular endothelial inflammation 认领 引用
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作者 Liting Huang Xingming Zhong +10 位作者 Longwei Yang Hongjing You Shengtao Xiong Ke Wang Lanting Fu Hecai Wang Liang Long Yunting Wang Haiyan Li Qiuhe Chen Yang Chen 《World Journal of Integrated Traditional and Western Medicine》 2026年第1期66-83,共18页
Objectives:The study aimed to investigate the efficacy and underlying mechanisms of Yang Mai Tong Luo formula(YMTLF)in the treatment of heart failure with preserved ejection fraction(HFpEF)by focusing on its ability t... Objectives:The study aimed to investigate the efficacy and underlying mechanisms of Yang Mai Tong Luo formula(YMTLF)in the treatment of heart failure with preserved ejection fraction(HFpEF)by focusing on its ability to alleviate microvascular endothelial inflammation.Methods:We analyzed the main components of YMTLF using ultra-performance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS).An HFpEF mouse model was established using high-fat diet and N-nitro-L-arginine methyl ester(L-NAME)stimulation and then treated with YMTLF for 10 weeks.Cardiac function of mice was assessed by echocardiography.Myocardial cross-sectional area was evaluated by wheat germ agglutinin(WGA)staining.The blood perfusion of hindlimb was analyzed by laser speckle.Network pharmacology and transcriptome analysis were employed to explore the potential mechanisms of YMTLF in addressing HFpEF.Immunofluorescence staining was used to analyze the expression levels of proteins related to microvascular inflammation.Results:A total of 27 principal components of YMTLF were characterized by UPLC-MS/MS.YMTLF reversed the body mass gain,improved heart function and myocardial hypertrophy of HFpEF mice.Specifically,YMTLF treatment reduced serum N-terminal probrain natriuretic peptide(NT-proBNP)levels from 622 to 319 pg/mL and decreased left ventricular posterior wall thickness in diastole(LVPWD)from 0.794 to 0.604 mm(P<0.05).Furthermore,it improved hindlimb blood perfusion(perfusion unit value increased from 156 to 226).It ameliorated the microvascular endothelial dysfunction(zonula occludens-1,intercellular adhesion molecule-1 and vascular cell adhesion molecule-1)and downregulated the expression levels of microvascular inflammation related proteins(interleukin-1β,F4/80,high mobility group box 1,transforming growth factor β1 and thrombospondin-1)(P<0.05).Conclusions:YMTLF exerted a therapeutic effect on HFpEF by ameliorating microvascular inflammation. 展开更多
关键词 Yang Mai Tong Luo formula(YMTLF) heart failure with preserved ejection fraction(HFpEF) vascular endothelial dysfunction inflammation transforming growth factorβ(TGF-β)
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Changes in endothelial morphology and ocular aberrations in pterygium 认领 引用
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作者 Sevgi Subasi Dilara Celikoglu +1 位作者 Dilara Pirhan Nursen Yuksel 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2026年第5期883-890,共8页
AIM:To compare changes in the corneal surface and endothelium,and to investigate their relationship with the horizontal length(HL),vertical length(VL),and depth of pterygium.METHODS:This study analyzed 34 eyes with un... AIM:To compare changes in the corneal surface and endothelium,and to investigate their relationship with the horizontal length(HL),vertical length(VL),and depth of pterygium.METHODS:This study analyzed 34 eyes with unilateral primary pterygium and compared them to the 34 fellow eyes.Topographic values,wavefront aberrations,and specular microscopy findings were assessed.In addition,correlation analyses were conducted between the HLs and VLs,as well as the depth of pterygium.RESULTS:The mean age of the patients was 60.18±11.36y(38.2%females).Uncorrected visual acuity(UCVA)was lower,and corneal astigmatism was higher in the pterygium group(P=0.006 and P<0.001,respectively).Simulated keratometry 1(simK1)measurements showed significant corneal flattening in the pterygium group(P=0.038).Notably,the HL of the pterygium(r=0.646,P<0.001)demonstrated a stronger correlation with corneal astigmatism than the VL(r=0.449,P=0.008).No significant correlation was observed between depth(r=-0.007,P=0.971)and corneal astigmatism.Furthermore,significant increases were noted in total higher-order aberrations(HOA;P=0.013),trefoil(P=0.002),tetrafoil(P=0.001),and highorder astigmatism(P<0.001)in the pterygium group.Mean point spread function(PSF)values were also significantly impaired in the pterygium group(P=0.007).Regarding endothelial parameters,the median endothelial cell density(ECD)was 2448.50(2176.00-2750.25 cells/mm2)in pterygium group,and 2554.00(2252.50-2890.00 cells/mm2)in the control group(P=0.289).No correlation was found between HS or VL and specular microscopy findings.However,a negative correlation was observed between depth and hexagonality(r=-0.381,P=0.026),and between depth and central corneal thickness(CCT;r=-0.422,P=0.013).CONCLUSION:The effect of pterygium on corneal aberrations is more strongly associated with its HL than with its VL.Depth do not affect aberrations,and pterygium has no significant effect on the ECD. 展开更多
关键词 pterygium corneal astigmatism corneal aberrations root mean square endothelial cell density
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Nuclear translocation of pyruvate kinase M2 drives high glucose-induced angiogenesis in retinal endothelial cells via the HIF-1α axis 认领 引用
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作者 Tian-Yi Liu Ya-Jing Tian +6 位作者 Peng-Zhou Kuai Yi-Sheng Luo Cheng-Wei Duan Tian-Peng Chen Xiao-Le Wang Dong-Mei Zhang Xin Cao 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2026年第5期858-868,共11页
AIM:To investigate the role of pyruvate kinase M2(PKM2)in high glucose(HG)-stimulated retinal endothelial cells and its underlying molecular mechanisms and signaling pathways in retinal angiogenesis.METHODS:Human reti... AIM:To investigate the role of pyruvate kinase M2(PKM2)in high glucose(HG)-stimulated retinal endothelial cells and its underlying molecular mechanisms and signaling pathways in retinal angiogenesis.METHODS:Human retinal microvascular endothelial cells(HRMECs)were cultured and divided into the following groups:normal glucose(NG,5.5 mmol/L),HG(30 mmol/L),HG with PKM2 knockdown(HG+shPKM2),and HG treated with the pharmacological activator TEPP‑46(HG+TEPP‑46).Cellular viability,proliferation,migration,and tube‑forming ability were assessed using CCK‑8,EdU,wound healing/Transwell,and Matrigel assays,respectively.The expression levels of PKM2,phosphorylated PKM2(p‑PKM2,Y105),hypoxia-inducible factor-1α(HIF‑1α),and vascular endothelial growth factor A(VEGFA)were detected by Western blotting.The oligomerization status of PKM2 was analyzed via native gel electrophoresis.The subcellular localization of PKM2 was examined by immunofluorescence and nuclear‑cytoplasmic fractionation.RESULTS:Under HG stimulation,the expression level of PKM2 was significantly increased(P<0.05).Knockdown of PKM2 was found to markedly suppress cell viability,proliferation,migration,and tube formation in HRMECs(P<0.05).Mechanistic studies revealed that phosphorylation of PKM2 at the Y105 site was promoted by HG treatment,which induced its dissociation from a tetramer to a dimer,thereby driving its nuclear translocation.Upon entering the nucleus,PKM2 was shown to exert critical non‑metabolic functions;it was physically bound to HIF‑1αand acted as its co‑activator,leading to significant upregulation of VEGFA expression(P<0.05).In contrast,the PKM2 activator TEPP‑46 effectively prevented dimerization and nuclear translocation of PKM2 by promoting its tetramerization.Consequently,the PKM2/HIF‑1αaxis‑mediated upregulation of VEGFA was blocked,ultimately resulting in the reversal of HG‑induced angiogenesis.CONCLUSION:HG influences retinal endothelial cell function by inducing PKM2 phosphor ylation,dimerization,and nuclear translocation.The shift in PKM2 phosphorylation and oligomerization status represents a key mechanism through which TEPP-46 reverses HGinduced angiogenesis. 展开更多
关键词 retinal endothelial cells glucose angiogenesis nuclear translocation pyruvate kinase M2 hypoxia-inducible factor-1α
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Silencing SLC31A1 attenuates high glucose plus copperinduced cuproptosis-like signaling,oxidative stress,and barrier dysfunction in human retinal microvascular endothelial cells 认领 引用
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作者 Ying Li Meng Chen Han-Guang Dong 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2026年第8期1461-1469,共9页
●AIM:To examine whether SLC31A1 knockdown protects human retinal microvascular endothelial cells(HRMECs)exposed to high glucose and copper.●METHODS:HRMECs were exposed to normal glucose(5 mmol/L)or high glucose(30 m... ●AIM:To examine whether SLC31A1 knockdown protects human retinal microvascular endothelial cells(HRMECs)exposed to high glucose and copper.●METHODS:HRMECs were exposed to normal glucose(5 mmol/L)or high glucose(30 mmol/L),with or without 50μmol/L CuSO4 during the final 6h,and transfected with control or SLC31A1 small interfering RNA.Cell viability(cell counting kit-8)and adenosine triphosphate(ATP)content were measured.Oxidative stress was assessed by glutathione/oxidized glutathione ratio,malondialdehyde,superoxide dismutase,catalase,and reactive oxygen species.Intracellular copper and mRNA levels of SLC31A1,ferredoxin 1,lipoic acid synthetase,dihydrolipoamide S-acetyltransferase(DLAT),and tight junction genes were quantified.SLC31A1 protein and lipoylated DLAT were detected by Western blotting.Endothelial barrier function was evaluated by fluorescein isothiocyanate-dextran permeability and transendothelial electrical resistance.●RESULTS:High glucose alone caused modest loss of viability,ATP depletion,increased oxidative stress,downregulation of tight junction genes,and mild barrier impairment,with minimal additional effect of SLC31A1 knockdown.Copper supplementation under high glucose induced marked intracellular copper overload,enhanced DLAT lipoylation,severe ATP loss,oxidative injury,and pronounced barrier dysfunction.SLC31A1 knockdown significantly reduced copper accumulation,lipoylation of DLAT,and oxidative stress,preserved ATP and viability,and partially restored tight junction gene expression and barrier function,although none of these parameters returned to normal glucose levels.●CONCLUSION:SLC31A1-dependent copper influx appears to contribute to cuproptosis-associated mitochondrial energy failure,oxidative stress,and barrier breakdown in high glucose-exposed retinal endothelial cells,indicating that SLC31A1 may represent a potential therapeutic target for diabetic retinal microvascular protection. 展开更多
关键词 SLC31A1 cuproptosis-like signaling diabetic retinopathy retinal microvascular endothelial cells oxidative stress
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Systemic outcomes of anesthesia method in anti-vascular endothelial growth factor therapy for retinopathy of prematurity:General vs topical 认领 引用
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作者 Asaad A Al Habsi Hilal K Al Mandhari +3 位作者 Anuradha S Ganesh Sana S Al Zuhaibi Nasra S Al Habsi Nouf H Al-Farsi 《World Journal of Clinical Pediatrics》 2026年第3期264-270,共7页
BACKGROUND The type of anesthesia needed while performing an anti-vascular endothelial growth factor(VEGF)injection in preterm infants with retinopathy of prematurity is not well standardized.In Oman,general anesthesi... BACKGROUND The type of anesthesia needed while performing an anti-vascular endothelial growth factor(VEGF)injection in preterm infants with retinopathy of prematurity is not well standardized.In Oman,general anesthesia(GA)remained the first choice by ophthalmologists treating retinopathy of prematurity(ROP)infants at the time of starting the study.Short-term systemic outcome in GA vs topical anesthesia(TA)is the primary outcome of this study.AIM To analyze the short-term systemic outcomes of GA in infants undergoing anti-VEGF injections vs bedside injections under TA.METHODS This is an observational study with historical comparison.Estimated sample size is 36(18 in each group),based on the anticipated rate of difference in the outcome between the two cohorts of 50%,type I error(α)probability of 5%,power of 80%,and the allocation ratio of 1:1.The statistical test considered was Fisher’s exact test.The calculation was done using the G*Power version 3.1.9.2.Infants were from two main tertiary hospitals in Oman.RESULTS A total of 36 infants with retinopathy of prematurity were enrolled in the study:18 in the retrospective(GA)cohort and 18 in the prospective(TA)cohort.The Primary outcome-the need for oxygen and/or respiratory support during the 48 hours post-procedure-occurred in 27.8%of the GA cohort,as compared to none of TA cohort(P value=0.045).Cost and duration of the procedure,including anesthesia,were noted to be higher in the GA group.Surgeons’preference revealed that 70%prefer topical vs 30%general in terms of safety,75%topical vs 25%general in terms of logistics,and 100%prefer topical in terms of cost and staff efforts.CONCLUSION TA is associated with a reduced need for oxygen and/or respiratory support within 48 hours post-procedure,and better performance in duration,cost,and surgeon preference compared to GA. 展开更多
关键词 Retinopathy of prematurity General anesthesia Topical anesthesia Anti-vascular endothelial growth factor injection
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