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Microglia overexpressing brain-derived neurotrophic factor promote vascular repair and functional recovery in mice after spinal cord injury 认领 引用 被引量：3
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作者 Fanzhuo Zeng Yuxin Li +6 位作者 Xiaoyu Li Xinyang Gu Yue Cao Shuai Cheng He Tian Rongcheng Mei Xifan Mei 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第1期365-376,共12页
Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in s... Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in spinal cord injury.Previous studies have shown that microglia can promote neuronal survival by phagocytosing dead cells and debris and by releasing neuroprotective and anti-inflammatory factors.However,excessive activation of microglia can lead to persistent inflammation and contribute to the formation of glial scars,which hinder axonal regeneration.Despite this,the precise role and mechanisms of microglia during the acute phase of spinal cord injury remain controversial and poorly understood.To elucidate the role of microglia in spinal cord injury,we employed the colony-stimulating factor 1 receptor inhibitor PLX5622 to deplete microglia.We observed that sustained depletion of microglia resulted in an expansion of the lesion area,downregulation of brain-derived neurotrophic factor,and impaired functional recovery after spinal cord injury.Next,we generated a transgenic mouse line with conditional overexpression of brain-derived neurotrophic factor specifically in microglia.We found that brain-derived neurotrophic factor overexpression in microglia increased angiogenesis and blood flow following spinal cord injury and facilitated the recovery of hindlimb motor function.Additionally,brain-derived neurotrophic factor overexpression in microglia reduced inflammation and neuronal apoptosis during the acute phase of spinal cord injury.Furthermore,through using specific transgenic mouse lines,TMEM119,and the colony-stimulating factor 1 receptor inhibitor PLX73086,we demonstrated that the neuroprotective effects were predominantly due to brain-derived neurotrophic factor overexpression in microglia rather than macrophages.In conclusion,our findings suggest the critical role of microglia in the formation of protective glial scars.Depleting microglia is detrimental to recovery of spinal cord injury,whereas targeting brain-derived neurotrophic factor overexpression in microglia represents a promising and novel therapeutic strategy to enhance motor function recovery in patients with spinal cord injury. 展开更多
关键词 angiogenesis apoptosis brain-derived neurotrophic factor colony stimulating factor 1 receptor inflammation microglia motor function spinal cord injury vascular endothelial growth factor
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SP7 transcription factor ameliorates bone defect healing in low-density lipoprotein receptor-related protein 5(LRP5)-dependent osteoporosis mice 认领 引用 被引量：1
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作者 Yue XI Qifeng JIANG +7 位作者 Wei DAI Chaozhen CHEN Yang WANG Xiaoyan MIAO Kaichen LAI Zhiwei JIANG Guoli YANG Ying WANG 《Journal of Zhejiang University-SCIENCE B》 SCIE CAS CSCD 2025年第3期254-268,共15页
Loss-of-function variants of low-density lipoprotein receptor-related protein 5(LRP5)can lead to reduced bone formation,culminating in diminished bone mass.Our previous study reported transcription factor osterix(SP7)... Loss-of-function variants of low-density lipoprotein receptor-related protein 5(LRP5)can lead to reduced bone formation,culminating in diminished bone mass.Our previous study reported transcription factor osterix(SP7)-binding sites on the LRP5 promoter and its pivotal role in upregulating LRP5 expression during implant osseointegration.However,the potential role of SP7 in ameliorating LRP5-dependent osteoporosis remained unknown.In this study,we used mice with a conditional knockout(c KO)of LRP5 in mature osteoblasts,which presented decreased osteogenesis.The in vitro experimental results showed that SP7 could promote LRP5 expression,thereby upregulating the osteogenic markers such as alkaline phosphatase(ALP),Runt-related transcription factor 2(Runx2),andβ-catenin(P<0.05).For the in vivo experiment,the SP7 overexpression virus was injected into a bone defect model of LRP5 c KO mice,resulting in increased bone mineral density(BMD)(P<0.001)and volumetric density(bone volume(BV)otal volume(TV))(P<0.001),and decreased trabecular separation(Tb.Sp)(P<0.05).These data suggested that SP7 could ameliorate bone defect healing in LRP5 c KO mice.Our study provides new insights into potential therapeutic opportunities for ameliorating LRP5-dependent osteoporosis. 展开更多
关键词 Gene therapy Low-density lipoprotein receptor-related protein 5(LRP5) Transcription factor osterix(SP7) Osteoporosis Defect healing
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Organelle symphony:Nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B in stroke pathobiology 认领 引用 被引量：1
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作者 Ziliang Hu Mingyue Zhao +4 位作者 Hangyu Shen Liangzhe Wei Jie Sun Xiang Gao Yi Huang 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第4期1483-1496,共14页
Strokes include both ischemic stroke,which is mediated by a blockade or reduction in the blood supply to the brain,and hemorrhagic stroke,which comprises intracerebral hemorrhage and subarachnoid hemorrhage and is cha... Strokes include both ischemic stroke,which is mediated by a blockade or reduction in the blood supply to the brain,and hemorrhagic stroke,which comprises intracerebral hemorrhage and subarachnoid hemorrhage and is characterized by bleeding within the brain.Stroke is a lifethreatening cerebrovascular condition characterized by intricate pathophysiological mechanisms,including oxidative stress,inflammation,mitochondrial dysfunction,and neuronal injury.Critical transcription factors,such as nuclear factor erythroid 2-related factor 2 and nuclear factor kappa B,play central roles in the progression of stroke.Nuclear factor erythroid 2-related factor 2 is sensitive to changes in the cellular redox status and is crucial in protecting cells against oxidative damage,inflammatory responses,and cytotoxic agents.It plays a significant role in post-stroke neuroprotection and repair by influencing mitochondrial function,endoplasmic reticulum stress,and lysosomal activity and regulating metabolic pathways and cytokine expression.Conversely,nuclear factor-kappa B is closely associated with mitochondrial dysfunction,the generation of reactive oxygen species,oxidative stress exacerbation,and inflammation.Nuclear factor-kappa B contributes to neuronal injury,apoptosis,and immune responses following stroke by modulating cell adhesion molecules and inflammatory mediators.The interplay between these pathways,potentially involving crosstalk among various organelles,significantly influences stroke pathophysiology.Advancements in single-cell sequencing and spatial transcriptomics have greatly improved our understanding of stroke pathogenesis and offer new opportunities for the development of targeted,individualized,cell typespecific treatments.In this review,we discuss the mechanisms underlying the involvement of nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B in both ischemic and hemorrhagic stroke,with an emphasis on their roles in oxidative stress,inflammation,and neuroprotection. 展开更多
关键词 inflammation nuclear factor erythroid 2-related factor 2 nuclear factor-kappa B organelles oxidative stress stroke
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Qiweizhigan granule ameliorates metabolic dysfunction-associated steatohepatitis by modulating the galectin 3/tumor necrosis factor receptor-associated factor 6-mediated ferroptosis 认领 引用 被引量：1
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作者 Yu-Nuo Yang Yun-Hong Sun +9 位作者 Ming-Zhe Zhu Yi-Rong Wang Meng Li Kai Wang Jing Ma Li Zhang Dan Hu Wen-Jun Zhou Guang Ji Yan-Qi Dang 《World Journal of Gastroenterology》 SCIE CAS 2026年第17期116-134,共19页
BACKGROUND Qiweizhigan granule(QWZG)is employed in clinical settings for the treatment of metabolic dysfunctionassociated steatohepatitis(MASH).However,the precise biological mechanisms underlying its therapeutic effe... BACKGROUND Qiweizhigan granule(QWZG)is employed in clinical settings for the treatment of metabolic dysfunctionassociated steatohepatitis(MASH).However,the precise biological mechanisms underlying its therapeutic effects are not yet fully elucidated.AIM To assess the efficacy and the mechanism of QWZG against MASH.METHODS Animal models were established,including normal group,a choline-deficient,L-amino acid-defined high-fat diet(CDAHFD)group,and low/medium/high-dose QWZG groups,as well as a rosiglitazone group.Through comprehensive biochemical,histopathological,RNA sequencing,and bioinformatics analyses,galectin 3(LGALS3)was identified as a critical target of QWZG in the treatment of MASH.The level of LGALS3 was quantitatively assessed and validated using Western blotting,real-time quantitative PCR,and immunofluorescence.The role and function of LGALS3 in inflammation and MASH progression were further investigated through gene knockdown,overexpression,iron assay,and transmission electron microscopy.RESULTS QWZG significantly ameliorated liver pathology by reducing steatosis,inflammation,and fibrosis.RNA sequencing analysis identified 1507 co-expressed differentially expressed genes among the CDAHFD,normal,and QWZG groups.Among these,LGALS3 was identified as one of the most significantly altered differentially expressed genes.Both mRNA and protein levels of LGALS3 were elevated in the CDAHFD group compared to the normal group,whereas treatment with QWZG reduced their levels.Analysis of Human Protein Atlas database indicated that LGALS3 was predominantly expressed in Kupffer cells,and was validated by real-time quantitative PCR and immunofluorescence.Furthermore,the level of LGALS3 was significantly increased in lipopolysaccharide-induced RAW264.7 cells,where its overexpression and recombinant LGALS3 protein both significantly enhanced the expression of interleukin-6,interleukin-1β,and tumor necrosis factor-α.LGALS3 overexpression significantly inhibited glutathione peroxidase 4(GPX4)expression,and exacerbated mitochondrial damage,whereas LGALS3 knockdown markedly increased GPX4 level,and significantly reduced the levels of both total iron and ferrous iron.QWZG treatment significantly reduced the levels of malondialdehyde and ferrous iron,increased the levels of superoxide dismutase and glutathione.In addition,QWZG treatment also significantly enhanced GPX4 expression.Mechanistically,LGALS3 knockdown was associated with reduced expression of tumor necrosis factor receptor-associated factor 6(TRAF6)and NOD-like receptor family pyrin domain containing 3,while its overexpression led to increased levels of these proteins.The TRAF6 inhibitor C25-140 effectively reversed the LGALS3-induced alterations in GPX4 expression and iron accumulation.Furthermore,QWZG treatment significantly decreased the levels of TRAF6 and NOD-like receptor family pyrin domain containing 3.CONCLUSION QWZG ameliorated the progression of MASH by modulating ferroptosis through the LGALS3/TRAF6/GPX4 axis. 展开更多
关键词 Qiweizhigan granule Metabolic dysfunction-associated steatohepatitis Galectin 3 Tumor necrosis factor receptorassociated factor 6 Ferroptosis
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Variations and major driving factors for soil nutrients in a typical karst region in Southwest China 认领 引用 被引量：2
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作者 Miaomiao Wang Hongsong Chen +1 位作者 Wei Zhang Kelin Wang 《Journal of Integrative Agriculture》 SCIE CAS CSCD 2026年第2期424-435,共12页
Understanding the spatial distributions and corresponding variation mechanisms of key soil nutrients in fragile karst ecosystems can assist in promoting sustainable development.However,due to the implementation of eco... Understanding the spatial distributions and corresponding variation mechanisms of key soil nutrients in fragile karst ecosystems can assist in promoting sustainable development.However,due to the implementation of ecological restoration initiatives such as land-use conversions,novel changes in the spatial characteristics of soil nutrients remain unknown.To address this gap,we explored nutrient variations and the drivers of the variation in the 0–15 cm topsoil layer using a regional-scale sampling method in a typical karst area in northwest Guangxi Zhuang Autonomous Region,Southwest China.Descriptive statistics,geostatistics,and spatial analysis were used to assess the soil nutrient variability.The results indicated that soil organic carbon(SOC),total nitrogen(TN),total phosphorus(TP),and total potassium(TK)concentrations showed moderate variations,with coefficients of variance being 0.60,0.60,0.71,and 0.72,respectively.Moreover,they demonstrated positive spatial autocorrelations,with global Moran's indices being 0.68,0.77,0.64,and 0.68,respectively.However,local Moran's index values were low,indicating large spatial variations in soil nutrients.The best-fitting semi-variogram models for SOC,TN,TP,and TK concentrations were spherical,Gaussian,exponential,and exponential,respectively.According to the classification criteria of the Second National Soil Census in China,SOC and TN concentrations were relatively sufficient,with the proportions of rich and very rich levels being up to 90.9 and 96.0%,respectively.TP concentration was in the mediumdeficient level,with the areas of medium and deficient levels accounting for 33.7 and 30.1%of the total,respectively.TK concentration was deficient,with the cumulative area of extremely deficient,very deficient,and deficient levels accounting for 87.6%of the total area.Consequently,the terrestrial ecosystems in the study area were more vulnerable to soil P and K than soil N deficiencies.Furthermore,variance partitioning analysis of the influencing factors showed that,except for the interactions,the single effect of other soil properties accounted more for soil nutrient variations than spatial and environmental variables.These results will aid in the future management of terrestrial ecosystems. 展开更多
关键词 dominant factor geostatistics karst ecosystem soil nutrient classification spatial variation
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A National Follow-up Study on the Effect of Health Protective Factors on Frailty Transition among Older Adults in China 认领 引用 被引量：1
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作者 Jing Shi Ziyi Zhou +12 位作者 Baiyu Zhou Yongkang Tao Yan Cen Luyao Zhang Sainan Li Ying Li Botao Sang Xiangfei Liu Qinan Ma Xuezhai Zeng Pulin Yu Jing Li Deping Liu 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2026年第3期270-284,共15页
Objective Frailty is becoming increasingly common among aging adults.Frailty transitionis shaped by biological,social,psychological,and environmental factors.This study investigated combined effects of protective fact... Objective Frailty is becoming increasingly common among aging adults.Frailty transitionis shaped by biological,social,psychological,and environmental factors.This study investigated combined effects of protective factors on frailty transition by constructing a Protection Index(PI)to guide targeted interventions.Methods Data were extracted from the 4th Sample Survey of the Aged Population in Urban and Rural China,including baseline(2017)and follow-up(2019)surveys.Frailty was assessed using the Frailty Index(FI),whereas the PI measured protective factors.Frailty transitions over 2 years were analyzed prospectively.Pearson’s correlation examined the relationship between FI and PI,and logistic regression assessed the effects of PI on frailty transitions.Results This study included 9,093 older adults.FI values increased with age and were higher in women,whereas PI values decreased with age and were higher in men.Over 2 years,56.2%of the participants showed a stable frailty status,14.2%improved,and 29.6%worsened.Negative transitions were more common than positive transitions,with transitions occurring most frequently between adjacent states.The PI was moderately negatively correlated with the FI(r=−0.349,P<0.001).A higher PI was associated with a lower risk of negative transitions among robust and prefrail individuals(OR=0.989,0.981,both P<0.05),but showed no significant effect among those with existing frailty.Conclusion Negative frailty transitions were more common with advancing age.Enhancing PI may help prevent negative frailty transitions among robust and pre-frail older adults,underscoring the value of early interventions. 展开更多
关键词 Frailty transition Frailty Older adults Protective factors Follow-up study National survey
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NAC transcription factor PpNAP4 modulates sucrose accumulation by activating the expression of PpSUS1 and PpSPS2 during peach ripening 认领 引用 被引量：1
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作者 Jieyu Dai Ze Xu +7 位作者 Zhouheng Fang Qiancheng Han Pei Shi Jingwen Zhu Lijun Cao Hangkong Liu Yanan Hu Caiping Zhao 《Horticultural Plant Journal》 SCIE CAS CSCD 2026年第6期1318-1330,共13页
Sugars are crucial in determining fruit quality and significantly affect the commercial value.Sucrose is the primary soluble sugar in ripe peach fruit.However,the regulatorymechanism of sucrose synthesis in peach frui... Sugars are crucial in determining fruit quality and significantly affect the commercial value.Sucrose is the primary soluble sugar in ripe peach fruit.However,the regulatorymechanism of sucrose synthesis in peach fruit,especially during natural ripening,remains largely unexplored.This study identified two structural genes of peach(Prunus persica,‘Jinlinghuanglu’),PpSUS1 and PpSPS2,whose expression was strongly correlated with sucrose accumulation.The transcription factors that regulated the expression of these two genes during peach fruit ripening were screened;and three NACs(NAM,ATAF1/2 and CUC2),whose expression also significantly correlated with sucrose accumulation,were identified.Notably,PpNAP4(NAC-like,activated by APETALA3/PISTILLATA)displayed the highest activation activity toward the PpSUS1 and PpSPS2 promoters.The direct binding activity was confirmed using luciferase imaging and electrophoretic mobility shift assays.The sucrose content and expression of sucrose synthesis-related genes significantly increased when PpNAP4 was overexpressed in peach fruit and the tomato nor mutant.Moreover,PpNAP4 functioned synergistically with PpNAP6 to modulate sucrose synthesis,and PpNAP4 targeted its own promoter and feedback-activated its own expression.This research unveils a novel regulatory mechanism controlling sucrose accumulation in peach fruit. 展开更多
关键词 Prunus persica Sucrose NAC transcription factor PpNAP4 PpSUS1 PpSPS2
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The regulatory network composed of phytohormones,transcription factors and non-coding RNAs is involved in the flavonoids biosynthesis of fruits 认领 引用 被引量：1
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作者 Xiaoyuan Zheng Xuejiao Zhang Fankui Zeng 《Horticultural Plant Journal》 SCIE CAS CSCD 2026年第3期497-508,共12页
Flavonoids,abundant in the fruits,are pivotal to their growth,development,and storage.In addition,they have significant beneficial effects on human health.Consequently,research is increasingly concentrating on the reg... Flavonoids,abundant in the fruits,are pivotal to their growth,development,and storage.In addition,they have significant beneficial effects on human health.Consequently,research is increasingly concentrating on the regulatory mechanisms governing flavonoid biosynthesis in fruits.Phytohormones are involved in the regulation of flavonoid biosynthesis.The abscisic acid,ethylene,jasmonic acid,cytokinins,and brassinosteroids promote flavonoid biosynthesis,while auxin negatively regulates flavonoid biosynthesis.Subsequently,transcription factors from the MYB,bHLH,WRKY,NAC,and bZIP families are pivotal in regulating flavonoid biosynthesis.In addition,non-coding RNAs(microRNA and lncRNA)also participate in the regulation of flavonoids biosynthesis.MicroRNAs are generally believed to negatively regulate flavonoid metabolism in fruits,while lncRNAs have the opposite effect.Furthermore,the interactions between plant hormones,transcription factors,and non-coding RNAs in fruit flavonoid biosynthesis were analyzed.Ultimately,a foundational regulatory network for fruit flavonoid biosynthesis was hereby established. 展开更多
关键词 Flavonoids biosynthesis Phytohormone Transcription factor Non-coding RNAs Regulation network Fruit
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Total flavonoid-and nerve growth factor-loaded gelatin-genipin hydrogel improves repair after spinal cord injury 认领 引用 被引量：1
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作者 Yu Liang Deshuang Xi +5 位作者 Yilin Teng Pan Liu Yanbing Feng Qiumei Huang Ming Gao Shaohui Zong 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3122-3129,共8页
Rat nerve growth factor and total flavonoids from hawthorn leaf contribute to the recovery of neurological function after spinal cord injury,including traumatic,non-traumatic spinal cord injuries.However,it remains ch... Rat nerve growth factor and total flavonoids from hawthorn leaf contribute to the recovery of neurological function after spinal cord injury,including traumatic,non-traumatic spinal cord injuries.However,it remains challenging to efficiently deliver nerve growth factor and total flavonoids from hawthorn leaf to spinal cord injury sites,ensure their sustained release,and minimize further damage.In the present study,we chose a biocompatible and biodegradable gelatin as the substrate,which was crosslinked with the natural biological crosslinker genipin to form a gelatin-genipin hydrogel carrier for the slow release of nerve growth factor and total flavonoids from hawthorn leaf in spinal cord injury sites.The prepared gelatin-genipin hydrogel had good injectable properties and photothermal effects.Furthermore,when the hydrogel with 2%genipin,200 ng/mL nerve growth factor,and 320μg/mL total flavonoids from hawthorn leaf was combined with near infrared irradiation,there was a slow release of total flavonoids from hawthorn leaf and nerve growth factor,reduced oxidative stress,an improved inflammatory microenvironment,and accelerated angiogenesis and axonal regeneration via inhibition of the nuclear factor kappa-B signaling pathway,thereby promoting recovery from spinal cord injury.Collectively,our results indicate that this new hydrogel may improve the prognosis of spinal cord injury,and may represent a new strategy for treating spinal cord injury. 展开更多
关键词 composited hydrogel hawthorn leaf total flavonoids nuclear factor kappa-B pathway photothermal effect reactive oxygen species spinal cord injury
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Overexpressing neurogenic differentiation factor 1 in Müller cells improves retinal function after optic nerve crush injury in adult mice 认领 引用 被引量：1
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作者 Liting Zhong Dashuang Yang +5 位作者 Xiu Han Haiyang Cheng Di Xu Wen Li Gong Chen Ying Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第8期3854-3862,共9页
Optic nerve injury leads to axonal degeneration and the death of retinal ganglion cells,which ultimately causes vision loss.Notably,current treatments are limited.In the present study,we explored whether neurogenic di... Optic nerve injury leads to axonal degeneration and the death of retinal ganglion cells,which ultimately causes vision loss.Notably,current treatments are limited.In the present study,we explored whether neurogenic differentiation factor 1(NeuroD1 or ND1)overexpression in retinal Müller cells may repair the retina after optic nerve crush in mice.Adult mice were subjected to optic nerve crush followed by intravitreal AAV-7m8-GFAP-GFP-ND1 virus injection.Immunofluorescent staining,multi-electrode array recording,electroretinogram,and visual behavior tests were then performed to examine retinal and optic nerve structure and retinal function at various post-optic nerve crush and virus injection times.Western blot analysis and quantitative reverse transcription polymerase chain reaction were performed to explore the possible mechanisms.Compared with the control virus,specific overexpression of ND1 in Müller cells greatly improved the light responses of retinal ganglion cells and retinal neurons in optic nerve crush-injured mice as early as 1-2 weeks post-virus injection and lasted for up to 4 weeks.Neuronal survival in the ganglion cell layer and synaptic connections in the inner retina were slightly improved at 2 weeks;however,visual behavior,retinal ganglion cell survival,and optic nerve structure were not improved.ND1 transiently enhanced glial cell-derived neurotrophic factor expression in the optic nerve crush-injured retina but hardly inhibited retinal inflammation within 2 weeks.Together,our data indicate that ND1 overexpression in Müller cells improves retinal function in the optic nerve crush-injured retina,and suggest that its neuroprotective effect may be caused by enhanced glial cell-derived neurotrophic factor release. 展开更多
关键词 glial cell-derived neurotrophic factor inflammation Müller cell NeuroD1 optic nerve injury retinal ganglion cell synaptic connection
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Techniques and factors for reducing chronic neuropathic pain: A review 认领 引用 被引量：1
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作者 Damien P.Kuffler 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第4期1353-1358,共6页
Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability... Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability. Even without apparent inflammation, injury sites are associated with increased inflammatory markers. This review focuses on how it might be possible to reduce neuropathic pain by reducing inflammation. Physiologically, pain is resolved by a combination of the out-migration of pro-inflammatory cells from the injury site, the down-regulation of the genes underlying the inflammation, up-regulating genes for anti-inflammatory mediators, and reducing nociceptive neuron hyperexcitability. While various techniques reduce chronic neuropathic pain, the best are effective on < 50% of patients, no technique reliably or permanently eliminates neuropathic pain. This is because most techniques are predominantly aimed at reducing pain, not inflammation. In addition, while single factors reduce pain, increasing evidence indicates significant and longer-lasting pain relief requires multiple factors acting simultaneously. Therefore, it is not surprising that extensive data indicate that the application of platelet-rich plasma provides more significant and longer-lasting pain suppression than other techniques, although its analgesia is neither complete nor permanent. However, several case reports indicate that platelet-rich plasma can induce permanent neuropathic pain elimination when the platelet concentration is significantly increased and is applied to longer nerve lengths. This review examines the primary triggers of the development and maintenance of neuropathic pain and techniques that reduce chronic neuropathic pain. The application of plateletrich plasma holds great promise for providing complete and permanent chronic neuropathic pain elimination. 展开更多
关键词 anti-inflammatory factors axon regeneration inflammatory pain nerve regeneration nerve repair pain elimination pain reduction platelet-rich plasma pro-inflammatory factors restoration of function
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Spatial-temporal landslide hazard analysis considering ecological and hydrological factors 认领 引用
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作者 ZHAO Zheng LAN Hengxing +2 位作者 LI Langping BAO Han LIU Shijie 《Journal of Mountain Science》 SCIE CSCD 2026年第4期1547-1563,共17页
Ecological factors,such as vegetation roots,can enhance soil shear strength,reduce surface runoff erosion,and improve slope stability.Conversely,heavy rainfall can rapidly saturate unsaturated soil,weakening shear str... Ecological factors,such as vegetation roots,can enhance soil shear strength,reduce surface runoff erosion,and improve slope stability.Conversely,heavy rainfall can rapidly saturate unsaturated soil,weakening shear strength.As such,both ecological and hydrological processes play critical roles in shallow slope failures.In this study,we propose a spatialtemporal landslide hazard model considering ecological and hydrological factors.Specifically,ecological factors are incorporated in convolution neural network as a spatial probability module,and hydrological factors are involved in infinite slope hydrological model as a temporal probability module,finally we integrated the spatial-temporal probabilities using integration module.A case study in the Hengduan Mountain Region demonstrated that the proposed model outperforms traditional models by achieving higher prediction accuracy,with an increase in the landslide hit index,demonstrating the effectiveness of involving ecological and hydrological factors in landslide hazard analysis,offering practical suggestions for landslide risk management. 展开更多
关键词 Landslide hazard Spatial probability Temporal probability Ecological factor Hydrological factor
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Tamarixetin suppresses neuronal ferroptosis in ischemic stroke rats by targeting and facilitating nuclear factor erythroid-2-related factor 2 expression 认领 引用
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作者 Yanqiu Yang Mingxia Fang +8 位作者 Qingqi Meng Yan Mi Libin Xu Hua Guo Yueyang Liu Mingzhong Li Nanik Siti Aminah Zipeng Gong Yue Hou 《Acupuncture and Herbal Medicine》 CAS CSCD 2026年第1期73-90,共18页
Objective:Neuronal ferroptosis has emerged as a promising therapeutic target for ischemic stroke.Tamarixetin,a natural dietary flavonoid,exerts protective effects against ischemic stroke by modulating neuroinflammator... Objective:Neuronal ferroptosis has emerged as a promising therapeutic target for ischemic stroke.Tamarixetin,a natural dietary flavonoid,exerts protective effects against ischemic stroke by modulating neuroinflammatory responses and mitigating oxidative stress.However,its potential role in regulating neuronal ferroptosis remains unclear.Methods:A rat model of middle cerebral artery occlusion and reperfusion and an erastin-treated SH-SY5Y cell model were used for in vivo and in vitro experiments,respectively.The neurological function of the rats was evaluated using a series of behavioral tests,the Garcia scoring system,and 2,3,5-triphenyltetrazolium chloride staining.Neuronal damage was detected via immunofluorescence staining and terminal deoxynucleotidyl transferase(TdT)-mediated deoxyuridine triphosphate(dUTP)nickend labeling.Commercial kits,western blotting,and coimmunoprecipitation were used to analyze neuronal ferroptosis and the activation of the Nuclear factor erythroid-2–related factor 2(Nrf2)signaling pathway.The direct target protein of tamarixetin was examined using the cellular thermal shift assay,drug affinity-responsive target stability assay,surface plasmon resonance,and molecular docking.Cellular Nrf2 was knocked down using small interfering RNA.Results:Tamarixetin mitigated the neurological dysfunctions of middle cerebral artery occlusion and reperfusion(MCAO/R)rats,including motor dysfunction,limb coordination impairment,neurological deficit,cerebral infarction,and reduced neuronal loss.Furthermore,it alleviated neuronal ferroptosis in vivo and in vitro by lowering the levels of iron ions,reactive oxygen species,malondialdehyde,and acyl-CoA synthetase long-chain family member 4 and upregulating the expression of superoxide dismutase,glutathione,glutathione peroxidase 4,heme oxygenase-1,and solute carrier family 7 member 11.Tamarixetin activated the Nrf2 signaling pathway by suppressing Keap1 protein expression,weakening the interaction between Keap1 and Nrf2,upregulating Nrf2 protein expression and nuclear translocation,and promoting antioxidant response element activity.Nrf2 is the direct binding protein of tamarixetin.It specifically interacts with amino acid residues at arginine 72,arginine 515,and lysine 518.The effects of tamarixetin on Nrf2 signaling pathway activation and neuronal ferroptosis inhibition were abrogated in Nrf2 knockdown cells challenged with erastin.Conclusions:Our findings not only identify tamarixetin as a novel ferroptosis inhibitor but also elucidate its mechanism of action via direct binding and Nrf2 pathway activation,providing a promising therapeutic candidate for ischemic stroke. 展开更多
关键词 Ferroptosis Ischemic stroke Tamarixetin Neuron Nuclear factor erythroid-2-related factor 2
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Interferon regulatory factor 4-releasing 3D-printed scaffolds enhance spinal cord repair by modulating macrophage polarization 认领 引用 被引量：1
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作者 Jianhao Wang Jiawei Du +5 位作者 Tuo Fang Di Zhang Yigang Lv Zhongju Shi Hengxing Zhou Shiqing Feng 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第8期3706-3716,共11页
Three-dimensional(3D)-printed hydrogel scaffolds are widely used in spinal cord injury repair,with gelatin methacrylate being particularly favored owing to its excellent biocompatibility.However,traditional scaffolds ... Three-dimensional(3D)-printed hydrogel scaffolds are widely used in spinal cord injury repair,with gelatin methacrylate being particularly favored owing to its excellent biocompatibility.However,traditional scaffolds have a small contact area with tissues and lack the ability to regulate the inflammatory microenvironment.Therefore,there is a need to develop smart scaffolds with drug delivery and immune regulation functions.In this study,a 3D-printed gelatin methacrylate scaffold was developed to deliver interferon regulatory factor 4 in a targeted and sustained manner.The scaffold showed good mechanical properties,biocompatibility,and sustained interferon regulatory factor 4 release.The sustained-release interferon regulatory factor 4 competitively bound to myeloid differentiation factor 88 to inhibit the pro-inflammatory effects of interferon regulatory factor 5,and activated the signal transducer and activator of transcription 6 pathway to promote M2 macrophage polarization,thereby facilitating neural regeneration and recovery of spinal cord function.This indicates that the constructed interferon regulatory factor 4-loaded 3D-printed methyl acrylate-modified gelatin scaffold can regulate macrophage polarization through the interferon regulatory factor 4/5 axis,improve the inflammatory microenvironment after spinal cord injury,and thus provide a new target for promoting neural regeneration. 展开更多
关键词 3D-printed scaffold inflammatory microenvironment interferon regulatory factor 4 JAK1/STAT6 signaling pathway macrophage polarization microglia nerve regeneration spinal cord injury
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Shenling Baizhu powder(参苓白术散)reduced the oxidative stress and mitochondrial damage during ulcerative colitis via the Kelch-like ECH-associated protein 1-NF-E2-related factor 2/nuclear factor kappa B pathway 认领 引用 被引量：1
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作者 ZHANG Quanhui ZENG Jinlan +3 位作者 SU Liang WANG Yi DENG Yongwen ZHANG Xiuchai 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2026年第3期584-593,共10页
OBJECTIVE:To explore the effects and relative mechanisms of Shenling Baizhu powder(参苓白术散,SBP)on ulcerative colitis(UC).METHODS:This study investigates the potential of SBP,a traditional Chinese herbal formula,in ... OBJECTIVE:To explore the effects and relative mechanisms of Shenling Baizhu powder(参苓白术散,SBP)on ulcerative colitis(UC).METHODS:This study investigates the potential of SBP,a traditional Chinese herbal formula,in attenuating inflammation and oxidative stress in UC.Applying both in vivo(rat)and in vitro(human colonic epithelial cells)models,we explored the anti-inflammation and oxidative stress effect of SBP,focusing on the Kelch-like ECHassociated protein 1-NF-E2-related factor 2uclear factor kappa B(KEAP1-NRF2/NF-κB)pathway and mitochondrial homeostasis.RESULTS:Results demonstrated that SBP administration significantly improved the health status of rats,with less intestinal injury,and reduced inflammatory cytokines(tumor necrosis factor-alpha,interleukin-1 beta,and interleukin-6)and oxidative stress(myeloperoxidase,malondialdehyde,and reactive oxygen species)both in vivo and in vitro.Moreover,SBP restored the inhibited KEAP1-NRF2/NF-κB signaling during inflammatory responses induced by dextran sulfate sodium or lipopolysaccharide,and decreased the expression level of the inflammatory molecule:NF-κB.Besides,SBP also helped to restore the mitochondrial dynamics,as evidenced by the recovery of mitochondrial membrane potential and mitofusin-2 levels.CONCLUSION:These findings suggest that SBP may offer a promising alternative therapy for managing UC,providing anti-inflammatory and antioxidant benefits as key molecular mechanisms. 展开更多
关键词 colitis ulcerative inflammation oxidative stress Kelch-like ECH-associated protein 1 NF-E2-related factor 2 NF-kappa B Shenling Baizhu powder
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Could deciphering cellular-mesenchymal epithelial transition factor/hepatocyte growth factor network dynamics unlock novel biomarker-driven therapies for colorectal cancer? 认领 引用
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作者 Jun-Kai Wen Jing Xia +3 位作者 Lu Yu Guo-Liang Xu Gang-Fu Ye Yu-Hua Lin 《World Journal of Gastrointestinal Oncology》 SCIE 2026年第4期15-33,共19页
Colorectal cancer(CRC)poses a substantial global health challenge.Its pathogenesis involves intricate genetic and signaling pathway aberrations,among which the cellular-mesenchymal epithelial transition factor(c-Met)/... Colorectal cancer(CRC)poses a substantial global health challenge.Its pathogenesis involves intricate genetic and signaling pathway aberrations,among which the cellular-mesenchymal epithelial transition factor(c-Met)/hepatocyte growth factor(HGF)axis functions as a pivotal regulatory hub.Encoded by a proto-oncogene,the transmembrane receptor c-Met is activated by HGF,driving CRC cell proliferation,migration,invasion,and metastasis via critical signal transduction cascades.The c-Met factor overexpression is observed in 30%-70%of CRC tumors.This review elucidates c-Met/HGF-mediated carcinogenesis,emphasizing its crosstalk with epidermal growth factor receptor,vascular endothelial growth factor,and insulin-like growth factor 1 receptor pathways.Notably,c-Met amplification contributes to epidermal growth factor receptor inhibitor resistance,increasing signaling network complexity.MicroRNA-1 and microRNA-137 modulate c-Met expression to suppress CRC progression,while advancements in c-Met-targeted molecular imaging facilitate precise diagnosis and treatment monitoring.Progress in c-Met/HGF-targeted therapies,including small-molecule inhibitors,monoclonal antibodies,and tyrosine kinase inhibitors,shows promise in suppressing tumors and overcoming resistance.Future efforts should focus on optimizing combination therapies,refining patient stratification via imaging,and addressing drug resistance to enable personalized,efficacious CRC treatments leveraging this axis. 展开更多
关键词 Clinical translation Cell signal transduction Colorectal cancer Hepatocyte growth factor Cellular-mesenchymal epithelial transition factor
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Interferon regulatory factor 1 enhances T cell differentiation in patients with myasthenia gravis 认领 引用 被引量：1
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作者 Yuebei Luo Yijun Ren +3 位作者 Zeyi Wen Zhaohui Luo Huan Yang Liqun Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3267-3280,共14页
Interferon regulatory factor 1 is involved in many autoimmune conditions and is increased in patients with myasthenia gravis.However,its function in myasthenia gravis remains unclear.Herein,we explored the function of... Interferon regulatory factor 1 is involved in many autoimmune conditions and is increased in patients with myasthenia gravis.However,its function in myasthenia gravis remains unclear.Herein,we explored the function of interferon regulatory factor 1 in myasthenia gravis,with an aim to understand the underlying mechanisms.Patients with myasthenia gravis who had acetylcholine receptor antibodies were included in the study.Peripheral blood lymphocytes were extracted from the included patients,and B lymphocyte subsets were isolated.Next,T and B cells from peripheral blood were co-cultured to explore the interferon regulatory factor 1-related mechanisms in myasthenia gravis.Chromatin immunoprecipitation experiments confirmed an interaction between interferon regulatory factor 1 and the CD180 promoter region.Dual-luciferase reporter gene confirmed the transcriptional activity of interferon regulatory factor 1 on CD180 promoter.In vitro results further indicated that interferon regulatory factor 1 promoted B cell activation and T cell differentiation via the inhibition of CD180.Interferon regulatory factor 1 recruited histone deacetylase 1 to inhibit CD180 transcription.Additionally,histone deacetylase 1 promoted B cell activation and T cell differentiation.Finally,in vitro experiments demonstrated that CD180 inhibited B cell activation and T cell differentiation by inhibiting the Toll-like receptor 4/mitogen-activated protein kinasesuclear factor-kappa B pathway.Collectively,our results suggest that interferon regulatory factor 1 enhances T cell differentiation by recruiting histone deacetylase 1 to block B cell CD180 transcription in myasthenia gravis via the Toll-like receptor 4/mitogen-activated protein kinasesuclear factor-kappa B pathway.Together,these findings indicate the important role of interferon regulatory factor 1 in myasthenia gravis and suggest its molecular mechanisms.They also provide new ideas and targets for diagnosing and treating myasthenia gravis,which will be both scientifically and clinically valuable. 展开更多
关键词 autoimmune condition B cell CD180 histone deacetylase 1 interferon regulatory factor 1 mitogen-activated protein kinase myasthenia gravis nuclear factor-kappa B T cell Toll-like receptor 4
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Global epidemiology of ovarian cancer:patterns,trends,and risk factors 认领 引用
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作者 Ruyuan Li Anqi Zhao +3 位作者 Meicen Liu Lingeng Lu Bin Li Hongmei Zeng 《Cancer Biology & Medicine》 SCIE CAS CSCD 2026年第7期958-973,共16页
Ovarian cancer was the eighth most frequently diagnosed cancer among women in 2022.The global age-standardized incidence rate of ovarian cancer decreased from 7.22/100,000 to 6.71/100,000 from 1990 to 2021.However,inc... Ovarian cancer was the eighth most frequently diagnosed cancer among women in 2022.The global age-standardized incidence rate of ovarian cancer decreased from 7.22/100,000 to 6.71/100,000 from 1990 to 2021.However,incidence trends varied across countries.Declining ovarian cancer incidence rates were reported in high-income countries,such as the United States,Austria,the Netherlands,and Norway,while there were increasing incidence rates in Africa and parts of Asia,including Japan and India.The global age-standardized mortality rate of ovarian cancer decreased from 4.73/100,000 to 4.06/100,000 between 1999 and 2021 with varying trends among countries.Moreover,the age-standardized 5-year net ovarian cancer survival rate in most countries remained<50%.Several specific factors related to ovarian cancer risk have been identified,including reproductive factors,use of oral contraceptives,anti-inflammatory diets,endometriosis,pelvic inflammatory disease,obesity,diabetes,and occupational asbestos exposure.No screening or prevention strategy has been proven effective in downstaging or reducing mortality from ovarian cancer in an average-risk population without a family cancer history or pathogenic variants.Indeed,risk-reducing salpingo-oophorectomy remains the gold standard for lowering the risk of ovarian cancer in high-risk individuals with hereditary mutations.This review provides a comprehensive overview of the epidemiology,risk factors,screening,and prevention of ovarian cancer,aiming to offer a global perspective on public health strategies for addressing the disease. 展开更多
关键词 Ovarian cancer epidemiology risk factors trend prevention screening
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HD-ZIP transcription factors:pivotal regulators of plant reproductive development 认领 引用
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作者 Jiakun Zheng Feng Wang +2 位作者 Yingxiao Mai Xingling Su Rui Xia 《Horticultural Plant Journal》 SCIE CAS CSCD 2026年第4期735-746,共12页
The HD-ZIP gene family,a group of plant-specific transcription factors,plays pivotal regulatory roles in various aspects of plant growth and development.Accumulating evidence has demonstrated the extensive involvement... The HD-ZIP gene family,a group of plant-specific transcription factors,plays pivotal regulatory roles in various aspects of plant growth and development.Accumulating evidence has demonstrated the extensive involvement of HD-ZIP members in regulating reproductive developmental processes.This review systematically summarizes both the structural characteristics of the four HD-ZIP subfamilies(Ⅰ-Ⅳ)and their distinct regulatory roles in plant reproductive development.Recent studies reveal that a conserved HD-ZIPⅠclade serves as a core regulator of key reproductive processes,ranging from spike development in monocots(e.g.,barley Vrs1 and maize GT1)to sex determination in dicots(e.g.,cucumber CmHB40 and persimmon MeGI).Meanwhile,members of other subfamilies(HD-ZIPⅡ-Ⅳ)contribute significantly to diverse reproductive processes including pistil development,floral organ formation,and anther development,among others.This review provides a comprehensive synthesis of HD-ZIP subfamily functions in reproductive development,integrating current knowledge while highlighting critical research gaps.These insights aim to provide theoretical foundations for functional characterization and potential applications of HDZIP reproductive regulators,while advancing our understanding of transcriptional regulation mechanisms in plant reproductive development. 展开更多
关键词 HD-ZIP Transcription factor HD-ZIPⅠ Reproductive development
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Long-term real-world PM2.5 exposure induces depression-like behaviors in mice by disrupting nuclear factor erythroid 2-related factor 2-mediated astrocyte-to-microglia communication 认领 引用
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作者 Nannan Huang Weiqing Shi +4 位作者 Cuishuang Dong Bin Li Yaohan Wang Hanqing Chen Xiaobo Li 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3238-3248,共11页
Long-term exposure to ambient fine particulate matter(PM2.5)may increase the risk of neurotoxicity in human populations.However,research studies on the underlying mechanisms of chronic PM2.5-induced depression-like be... Long-term exposure to ambient fine particulate matter(PM2.5)may increase the risk of neurotoxicity in human populations.However,research studies on the underlying mechanisms of chronic PM2.5-induced depression-like behaviors,and potential therapeutical strategies,remain scarce.In the present study,after long-term exposure to real-world PM2.5 for 15 weeks,male mice displayed depression-like behaviors,which were revealed using the open field and sucrose preference tests.Mechanistically,chronic PM2.5 exposure promoted astrocytic A1 polarization and disrupted reduction-oxidation balance in the mouse hippocampus.Furthermore,PM2.5-exposed mice displayed pathological damage to hippocampal neurons as well as the inhibition of nuclear factor erythroid 2-related factor 2 signaling.Astrocytic ablation of nuclear factor erythroid 2-related factor 2 exacerbated PM2.5-induced hippocampal neuronal injury in mice via the disruption of astrocyte-to-microglia communication;this finding was confirmed in mice with bilateral and unilateral hippocampal astrocytic Nfe2l2 knockdown.Importantly,the upregulation of nuclear factor erythroid 2-related factor 2 activation by procyanidin significantly ameliorated PM2.5-induced depression-like behaviors through the remodeling of astrocyte-to-microglia communication.Together,our findings shed light on the important role of hippocampal astrocytic nuclear factor erythroid 2-related factor 2 activation for maintaining astrocyte-to-microglia communication,and indicate potential research avenues for therapeutic strategies against PM2.5-induced depresson-like behaviors. 展开更多
关键词 air pollution astrocyte-to-microglia communication depression-like behaviors fine particulate matter(PM2.5) neurotoxicity nuclear factor erythroid 2-related factor 2 oxidative stress procyanidins
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