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Heat stress induced testicular impairment is related to orchitis and complement activation in Rongchang boars 认领 引用
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作者 Xiangyuan Ma Wenxue Shen +11 位作者 Junhao Ni Xihao Luo Lianqiang Che Bin Feng Lun Hua Yong Zhuo Zhengfeng Fang Shengyu Xu Jian Li Xuemei Jiang Yan Lin De Wu 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2026年第1期488-499,共12页
Background Heat stress(HS)is posing as a tremendous threat to the swine industry,due to the thermos-sensitive gonads of boars.Testes are immune-privileged organs in which spermatogenesis needs to remain undisturbed,wh... Background Heat stress(HS)is posing as a tremendous threat to the swine industry,due to the thermos-sensitive gonads of boars.Testes are immune-privileged organs in which spermatogenesis needs to remain undisturbed,whereas immune cells are thermo-sensitive,especially macrophages,which are the most abundant testicular immune cells.Our study aimed to unveil the underlying immune responses and assess their consequences on the semen quality of boars under HS.The results will aid in addressing environmental temperature-related seasonal infertility and in selecting the best boar for use in artificial insemination.Methods The 3-week experiment assigned 268-week-old Rongchang male pigs into thermal neutral pair-feed(TN-PF)and HS groups.During the last 2 weeks,which served as the HS period,the HS group was subjected to 14-day 35±1℃,while the TN-PF group was kept at 26±1℃.Pig gonad tissues were sampled at the end of HS period for assessments and measurements.Results Our findings confirmed HS-related reactions such as elevated respiration rate(P<0.05)and elevated heat shock protein 60(HSP60;P<0.05)and heat shock protein 90(HSP90;P<0.05)expression levels.Sperm motility(P=0.06)and progressive sperms(P=0.08)were decreased under HS as was a significant reduction in average straight-line velocity(VSL;P<0.05).Additionally,total abnormality levels increased(P<0.05).Fibrosis,caspase-3 expression,and accumulations of tumor necrosis factor-α(TNF-α;P<0.05)and interleukin-1β(IL-1β;P<0.05),along with an elevated macrophage composition(P<0.05)characterized the orchitis under HS.Single cell RNA sequencing(scRNA-seq)revealed fluctuations in engulfing and inflammatory signals in testicular macrophages(TMs).In particular,the complement cascade was promoted by CD163+macrophages,resulting in membrane attack complex(C5b-9)assembly(P<0.05).Linear regressions further revealed a negative correlation between C5b-9 and sperm motility(P<0.05),as well as near-negative correlations between the C5b-9 and both progressive motility(P=0.08)and VSL(P=0.06).Conclusions Our findings highlighted the relationship between HS,the onset of orchitis,and the activation of the complement system,all of which decreased the boar semen quality. 展开更多
关键词 Boar Complement Heat stress Macrophage Orchitis Semen quality Testis
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Targeting adipocyte ESRRA alleviates osteoarthritis via interrupting inter-organelle crosstalk of complement C3-CFDMAC cascade 认领 引用
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作者 Tongling Huang Zihui Wang +13 位作者 Lu Gao Jun Gao Zhaocheng Lu Pengda Li Chon Him Choy Zhuolei Yuan Yanting Zhong Chang-An Geng Huaiyu Wang Kelvin W.K.Yeung Bin Li Haobo Pan Di Chen Min Guan 《Bone Research》 SCIE CAS CSCD 2026年第3期861-878,共18页
Osteoarthritis is an aging-related systemic disease involving the crosstalk of multiple organsissues in metabolism and inflammation,yet little is known about the contribution of liver and marrow adipose tissue(MAT).He... Osteoarthritis is an aging-related systemic disease involving the crosstalk of multiple organsissues in metabolism and inflammation,yet little is known about the contribution of liver and marrow adipose tissue(MAT).Here we show that MAT-derived complement factor D(CFD)and component 3(C3)derived from steatotic liver coordinately drive excessive alternative complement activation,resulting in cartilage damage in mice during aging and metabolic disorders.Mechanistically,estrogen-related receptorα(ESRRA)transcriptionally upregulates CFD responding to bone marrow adipocytes(BMAds)expansion.Inhibition of ESRRA/CFD signaling in BMAds blocks the chondrocyte senescence and catabolism triggered by C3 that is released from steatotic hepatocyte,interrupting C3-CFD-MAC cascade,thereby suppressing ERK1/2 phosphorylation and mitochondrial dysfunction.Adipocyte-specific ablation or pharmacological inhibition of ESRRA reduces CFD levels particularly in adipocyte-rich bone marrow,attenuating osteoarthritis progression in aged mice.Our findings highlight a key liver-MAT-cartilage axis bridged by C3-CFD-MAC pathway,raising the potential for adipocyte ESRRA-targeting therapies for aging-related metabolic osteoarthritis. 展开更多
关键词 steatotic liver cartilage damage excessive alternative complement activationresulting adipocyte Osteoarthritis Mitochondrial dysfunction Esrra Cfd
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Defect-complementation homologous recombination:A novel strategy for precise genome engineering of virulent phages 认领 引用
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作者 Hailin Zhang Yueyue Song +6 位作者 Wenyue Liu Xiaoqing Zheng Xiaodong An Chao Li Weihua Chen Hailong Wang Yuran Zhang 《Synthetic and Systems Biotechnology》 SCIE CSCD 2026年第2期59-70,共12页
Engineered bacteriophages(phages)have been developed to overcome the limitations of natural phage therapies and serve as precision-targeted agents against drug-resistant bacterial infections.However,their application ... Engineered bacteriophages(phages)have been developed to overcome the limitations of natural phage therapies and serve as precision-targeted agents against drug-resistant bacterial infections.However,their application has been constrained by the low efficiency of existing genome-editing tools,largely because of the absence of effective selection markers.This study proposed a novel strategy,termed defect-complementation homologous recombination(DCHR),for precise phage genome editing.In this approach,CRISPR-Cas9 cleaves a donor plasmid in host cells to release a linear donor template carrying homology arms,an essential phage gene used as a selection marker,and two lox sites.The donor template undergoes homologous recombination with the genome of essential gene-deficient phage,thereby enabling targeted genome modifications.Using DCHR,we successfully generated large genomic deletions(1.48-kb gp0.4–0.7 and 1.02-kb gp4.3–4.7),achieved gene insertion(3.08-kb lacZ),and introduced a single-base substitution(TGA to TAA)in the stop codon of gp9 within the same T7 phage genome,all with 100%accuracy.The significant advantages of DCHR are as follows:(i)High-efficiency screening:Only progeny phages derived from successful homologous recombination retain viability and replicative capacity,thereby greatly simplifying recombinant isolation.(ii)Editing flexibility:Unlike CRISPR-Cas systems,DCHR cannot be constrained by protospacer adjacent motif dependence and allows modifications across diverse genomic loci.(iii)High recombination efficiency:DCHR can achieve a recombinant phage titer of 3.1×105 PFU mL−1(plaque-forming units per mL)without relying on exogenous homologous recombination systems.In summary,DCHR demonstrates potential as a precise and efficient general genome-editing tool that facilitates design of engineered phages and advances functional genomic studies. 展开更多
关键词 Genetic complementation Phage genome engineering Cre-lox Phage genetic manipulation Homologous recombination
Complement C3a Suppresses Spinal Cord Neural Stem Cell Activation by Inhibiting UCHL1 via the NF-κB p65/Nrf2 Pathway 认领 引用
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作者 Lu Ding Xinyue Li +2 位作者 YaQin Guo Feng-Quan Zhou David Y.B.Deng 《Neuroscience Bulletin》 SCIE CAS CSCD 2026年第1期153-174,共22页
Activation of spinal cord neural stem cells(NSCs)and subsequent neurogenesis holds a promising alternative for spinal cord injury(SCI)repair.Our previous study demonstrated that complement C3a,derived from reactive as... Activation of spinal cord neural stem cells(NSCs)and subsequent neurogenesis holds a promising alternative for spinal cord injury(SCI)repair.Our previous study demonstrated that complement C3a,derived from reactive astrocytes,inhibits NSC proliferation by suppressing protein aggregate clearance through the deubiquitinating enzyme ubiquitin carboxy-terminal hydrolase L1(UCHL1)-proteasome system post-SCI.However,the potential molecular mechanism by which C3a modulates NSC activation via this pathway remains unclear.Here,we revealed that C3a/C3a receptor(C3aR)signaling activated NF-κB p65,which in turn inhibited Nrf2 activity and UCHL1 expression,resulting in diminished proteasome activity and the accumulation of protein aggregates,and ultimately impaired NSC activation.Both knockdown of NF-κB p65 and Nrf2 upregulation restored UCHL1 expression and proteasome activity in vitro,promoting NSC activation by enhancing protein aggregate clearance.Mechanistically,we found that NF-κB p65 regulated Nrf2 activity through a dual mechanism:(1)promoting Keap1-dependent ubiquitination and proteasome degradation of Nrf2;(2)inhibiting protein kinase C-mediated Nrf2 phosphorylation and nuclear translocation.Using the dual-luciferase reporter assay and chromatin immunoprecipitation(ChIP)analysis,we further identified UCHL1 as a direct transcriptional target of Nrf2.Importantly,in vivo experiments using SCI mice confirmed that either C3aR blockade,NF-κB p65 knockdown,or Nrf2 overexpression could rescue SCI-induced UCHL1 downregulation.Together,this study uncovers the C3a-NF-κB p65-Nrf2-UCHL1-proteasome axis as a critical regulator of NSC activation after SCI.This may provide novel molecular targets and intervention strategies for SCI repair. 展开更多
关键词 Complement C3a Neural stem cell activation UCHL1 NF-κB p65/Nrf2 pathway Protein aggregation clearance Spinal cord injury
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Machine learning identifies complement factor I as a shared mediator of periodontitis and ossification of posterior longitudinal ligament 认领 引用
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作者 Yu-Nan Man Lu-Yang Zhong +1 位作者 Yue-Liang Wen Mao-Lin He 《World Journal of Orthopedics》 2026年第3期133-151,共19页
BACKGROUND The clinical co-occurrence of periodontitis and ossification of the posterior longitudinal ligament(OPLL)suggests shared pathophysiological mechanisms,which remain poorly understood.AIM To elucidate the key... BACKGROUND The clinical co-occurrence of periodontitis and ossification of the posterior longitudinal ligament(OPLL)suggests shared pathophysiological mechanisms,which remain poorly understood.AIM To elucidate the key molecular and cellular mechanisms between periodontitis and OPLL.METHODS Transcriptomic datasets for human periodontitis and OPLL were integrated.We performed differential gene expression analysis,weighted gene co-expression network analysis,and cross-dataset meta-analysis.A comprehensive machine learning framework incorporating 10 algorithms was applied to identify core genes,with model interpretability assessed via SHapley Additive exPlanations.Single-cell RNA sequencing data from periodontitis tissues were used to validate cell-type-specific expression,and functional enrichment analyses were conducted to elucidate relevant pathways.RESULTS Multi-step analysis identified complement factor I(CFI)as a principal contributor to both conditions.CFI expression was consistently upregulated and demonstrated strong discriminatory capacity for periodontitis.At single-cell resolution,endothelial cells within the periodontitis microenvironment were observed to express CFI.Functional enrichment analysis indicated that CFI-positive cells were involved in pathways related to cell adhesion(focal adhesion,adherens junctions),inflammatory signaling(PI3K-Akt pathway),and bacterial infection responses.CONCLUSION CFI was identified as a pivotal node connecting periodontitis and OPLL,revealing novel mechanisms and suggesting its potential as a biomarker and therapeutic target. 展开更多
关键词 Ossification of the posterior longitudinal ligament Periodontitis Complement factor I Discriminatory biomarker Machine learning Transcriptome Single-cell RNA sequencing
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Trace element-dictated exosome modules and self-adaptive dual-network hydrogel orchestrate diabetic foot regeneration through complement-mitochondria-autophagy circuitry 认领 引用 被引量：1
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作者 Shuang-Qing Wang Ming-Ji Jin +11 位作者 Ze-Ke Guo Dong-Ri Shen Li-Na Jin Fang Cheng Yan-Ru Zhao Teng Liu Yu-Cai Li Nuo-Ya Wang Ling-Qing Chen Wei Huang Xiu-Quan Quan Zhong-Gao Gao 《Military Medical Research》 SCIE CAS CSCD 2026年第4期559-587,共29页
Background:Diabetic foot ulcers(DFU),perpetually trapped in a vicious cycle of inflammation and ischemia,remain a significant clinical challenge.Exosomes(Exo)therapy holds promise for tissue repair,yet its functional ... Background:Diabetic foot ulcers(DFU),perpetually trapped in a vicious cycle of inflammation and ischemia,remain a significant clinical challenge.Exosomes(Exo)therapy holds promise for tissue repair,yet its functional potency and delivery efficiency are often limited.Methods:We proposed an integrated strategy combining trace elements(TE)programming,Exo engineering,and intelligent delivery to overcome both functional and delivery constraints.Multiple TE(Fe,Mg,Zn,Mn,and Se)were incorporated into a three-dimensional(3D)dynamic culture system to construct high-activity engineered Exo(3D-TE-Exo).The biological mechanisms were explored via transcriptomics,mitochondrial function assays,and oxidative stress analyses.A dual-network hydrogel,incorporating dynamic Schiff base bonds and ultraviolet(UV)-triggered disulfide bond reorganization,was developed for precise and sustained Exo release in vivo.Results:3D-TE-Exo achieved a yield of 1.9×1012particles/ml,representing a 29-fold increase over conventional culture(6.5×1010particles/ml).These Exo modulated the complement pathway,restored mitochondrial membrane potential,enhanced adenosine triphosphate(ATP)production,and activated autophagy,thereby alleviating oxidative stress,with complement 1q binding protein(C1QBP)identified as a key mediator.The hydrogel enabled prolonged Exo retention and controlled release at the wound site.In DFU rat models,this system achieved 89.71%wound closure by day 14,significantly higher than the 50.64%observed in controls.Conclusions:This study presents a synergistic approach integrating engineered Exo and smart biomaterials to accelerate DFU healing.The platform offers a multi-target intervention strategy with strong translational potential for the clinical management of chronic wounds. 展开更多
关键词 Exosomes(Exo) Hydrogel Trace element Diabetic foot ulcers(DFU) Complement 1q binding protein(C1QBP)
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Identification and screening of bioactive peptides against nephropathy derived from Mantidis Oötheca based on complement C3 inhibition 认领 引用
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作者 Shanshan Li Peiling Liu +3 位作者 Tiantian Zhang Shujun Jiang Faren Xie Yanliang Zhang 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2026年第1期100-111,共12页
Insects represent emerging sources of bioactive peptides and functional materials.Mantidis Oötheca(Sang-Piao-Xiao in Chinese,SPX)serves as an insect-derived medicine for treating kidney disease.This study demonst... Insects represent emerging sources of bioactive peptides and functional materials.Mantidis Oötheca(Sang-Piao-Xiao in Chinese,SPX)serves as an insect-derived medicine for treating kidney disease.This study demonstrated that supernatant(SPX)improved kidney function in adriamycin(ADR)-induced nephropathy mice model.Transcriptomic analysis revealed that SPX inhibited complement activation by targeting the MASP1-C3/C3a receptor(C3aR)pathway.Peptidomic analysis identified 304 peptides from SPX,with 49 peptides selected for evaluation using prediction tools and molecular docking with complement core protein C3.Three peptides(PMGFPFDR,FNDPK,AAQFFNR)exhibiting docking scores below-8.0 were synthesized to verify complement inhibition and anti-fibrotic activities.The synthetic peptide AAQFFNR demonstrated complement inhibitory activity,with an inhibitory complement hemolytic 50%(ICH50)value of 24.54μmol·L-1,and exhibited superior protective effects in ADR-induced HK-2 cells.Surface plasmon resonance(SPR)assay revealed direct interaction between AAQFFNR and complement C3 with Kdvalue of 16.8μmol·L-1.The reno-protective effect of AAQFFNR was subsequently verified in ADR-induced mice.This research provides initial evidence that complement C3-inhibiting peptides from insects demonstrate potential in preventing nephropathy through in silico and in vivo validation approaches. 展开更多
关键词 Mantidis Oötheca Nephropathy Complement C3 Peptide screening
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Identification and validation of fecal complement component 3 and fibronectin as potential biomarkers for monitoring disease activity in ulcerative colitis based on a mouse model 认领 引用
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作者 Yangyun Guo Ziheng Yan +4 位作者 Jingyu Ye Ruifu Yang Yajun Song Hui Yue Yong Zhao 《Animal Models and Experimental Medicine》 CAS CSCD 2026年第7期1292-1301,共10页
Background:Ulcerative colitis(UC)is a typical inflammatory bowel disease requiring long-term management.Although fecal calprotectin(FC)is widely employed for assessing disease activity,it is still considered insuffici... Background:Ulcerative colitis(UC)is a typical inflammatory bowel disease requiring long-term management.Although fecal calprotectin(FC)is widely employed for assessing disease activity,it is still considered insufficient as a standalone tool.New biomarkers are needed to better predict risk and comprehensively reflect biological pathways.This study aimed to identify potential fecal biomarkers to monitor disease activity in UC.Methods:C57BL/6J mice were exposed to dextran sulfate sodium(DSS)treatment for 7 days.Feces were collected and subjected to proteomic analysis and enzyme-linked immunosorbent assay(ELISA).Mouse colon tissues were subjected to histopathological and immunofluorescence analyses.The correlations between the selected fecal proteins and disease severity were evaluated and compared with FC.Results:Proteomic analysis revealed increases in fecal complement component 3(C3)and fibronectin(FN)in the DSS group.Next,we measured fecal C3 and FN levels in mice using ELISA.Significant elevation in C3 and FN levels was observed as early as day 1 after DSS treatment,preceding the increase in FC.Both fecal C3 and FN demonstrated significant correlations with disease activity,with C3 exhibiting a stronger correlation than FC.Using immunofluorescence,we observed distinct C3 and FN expressions in both the colonic tissues and the intestinal lumen.Conclusion:These findings demonstrate that fecal C3 and FN are promising candidate biomarkers for monitoring UC disease activity,and their utility requires further validation in other colitis models and human cohorts. 展开更多
关键词 complement component 3(C3) disease activity fibronectin mouse model ulcerative colitis
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Niu Huang mitigates dextran sulfate sodium-induced colitis by modulating farnesoid X receptor activation and the complement 3/NLRP3 signaling pathway 认领 引用
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作者 Juan Shi Chong-Yang Ma +6 位作者 Xiao-Hui Zhang Kun-Jing Liu Jin-Ying Liu Qing-Guo Wang Xue-Qian Wang Fa-Feng Cheng Tian Xu 《World Journal of Gastroenterology》 SCIE CAS 2026年第17期135-155,共21页
BACKGROUND Ulcerative colitis(UC)is a chronic inflammatory bowel disease for which effective therapies are lacking.Niu Huang(NH)is a traditional Chinese medicine used for inflammatory disorders.However,its protective ... BACKGROUND Ulcerative colitis(UC)is a chronic inflammatory bowel disease for which effective therapies are lacking.Niu Huang(NH)is a traditional Chinese medicine used for inflammatory disorders.However,its protective effect on UC and its underlying mechanisms are unknown.AIM To uncover the mechanisms underlying the anti-colitis effects of the NH.METHODS Network pharmacology was applied to predict the active ingredients and targets of NH.Experimental validation was conducted in a dextran sulfate sodium-induced murine colitis model.The therapeutic efficacy was assessed using symptoms,histopathology,quantitative polymerase chain reaction,western blotting,immunohistochemistry and enzyme linked immunosorbent assay,while the underlying mechanism was investigated through integrated transcriptomic and proteomic analyses.In addition,the critical role of farnesoid X receptor(FXR)in mediating the effects of NH was validated using the FXR inhibitor guggulsterone and Fxr-/-mouse models.RESULTS Network pharmacology revealed that the bioactive component of NH is bile acid.Our animal experiments demonstrated that NH treatment significantly alleviated colitis symptoms and pathological damage.NH preserved intestinal mucosal integrity by upregulating occludin,claudin3,E-cadherin and leucine rich repeat containing G protein-coupled receptor 5 expression.Transcriptomic and proteomic analyses revealed that bile secretion,the nuclear factor kappa B signaling pathway and the complement and coagulation cascade pathway are key targets of NH.Western blotting confirmed that NH increased FXR levels and reduced P65,complement component 3(C3)and NOD-like receptor family pyrin domain containing 3(NLRP3)expression.Furthermore,experiments using Fxr-/-mice and the FXR antagonist revealed that FXR is a pivotal target through which NH attenuates UC.Mechanistic analysis revealed that the effects of NH on UC are mediated by the modulation of targets involved in the activation of FXR and the subsequent inhibition of C3/NLRP3 activation.CONCLUSION This study demonstrates the therapeutic effects of NH on UC.Mechanistically,NH acts by activating FXR,which subsequently inhibits the nuclear factor kappa B pathway to reduce C3 accumulation and suppress excessive NLRP3 inflammasome activation in colon tissue. 展开更多
关键词 Niu Huang Ulcerative colitis Network pharmacology Farnesoid X receptor Complement component 3/NOD-like receptor family pyrin domain containing 3 signaling pathway Inflammation
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Successful term pregnancy after renal transplant in end-stage renal disease with complement factor H-related mutation:A case report 认领 引用
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作者 Manish Ramesh Balwani Amit Pasari +13 位作者 Pranjal Kashiv Chaitanya Shembekar Manisha Shembekar Shubham Dubey Vijay Jeyachandran Sunny Malde Sushrut Gupta Twinkle Pawar Priyanka Tolani Mohit Kurundwadkar Prasad Gurjar Kapil Sejpal Charulata Bawankule Vivek B Kute 《World Journal of Transplantation》 2026年第1期256-262,共7页
BACKGROUND Complement-mediated thrombotic microangiopathy(TMA)is a rare endothelial injury syndrome caused by dysregulated activation of the alternative complement pathway,often linked to genetic abnormalities in comp... BACKGROUND Complement-mediated thrombotic microangiopathy(TMA)is a rare endothelial injury syndrome caused by dysregulated activation of the alternative complement pathway,often linked to genetic abnormalities in complement factor H(CFH),complement factor I,or complement factor H-related(CFHR)proteins.Both renal transplantation and pregnancy are independent triggers for recurrence.This case highlights a genetically high-risk patient who achieved a successful term pregnancy after renal transplantation without complement inhibition,emphasizing individualized risk stratification,close surveillance,and multidisciplinary management for favourable maternal and graft outcomes.CASE SUMMARY A 32-year-old woman with end-stage renal disease secondary to genetically confirmed complement-mediated TMA—homozygous CFH exon 17 deletion and CFHR3-CFHR1 duplication—was maintained on dialysis for 2.5 years before undergoing a successful live-donor kidney transplant from her mother.Post-transplant immunosuppression included tacrolimus,mycophenolate mofetil,and prednisolone,later modified to azathioprine during pregnancy planning.One-year post-transplant,she conceived spontaneously.Pregnancy was complicated by transient gestational hypertension,controlled with nifedipine,labetalol,and amlodipine.Proteinuria remained<150 mg/day;white blood cell counts 5.8-7.2×109/L without cytopenia.Serum creatinine ranged 0.9-1.1 mg/dL,and tacrolimus trough levels 5-7 ng/mL.At 36 weeks,she delivered a healthy 3 kg infant by elective caesarean section.Postpartum follow-up at three months confirmed stable maternal and graft function.CONCLUSION High-risk complement-mediated TMA patients can achieve successful pregnancy post-transplant through individualized care without mandatory complement blockade. 展开更多
关键词 Complement-mediated thrombotic microangiopathy CFH exon 17 deletion CFHR3-CFHR1 duplication Renal transplantation High-risk pregnancy Complement dysregulation Eculizumab-free management Atypical hemolytic uremic syndrome Case report
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The Extremal Graphs for the Spectral Radii of Complements of Graphs with Cut Vertices 认领 引用
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作者 Chen Xu Gao Guangyuan 《Journal of Mathematical Research with Applications》 CSCD 2026年第4期435-441,共7页
The adjacency matrix A(G)of a connected simple graph G is a symmetric(0,1)-matrix with real eigenvalues λ1≥λ2≥…≥λn.The maximum eigenvalueλ1 is called the spectral radius of G.In this paper,we characte... The adjacency matrix A(G)of a connected simple graph G is a symmetric(0,1)-matrix with real eigenvalues λ1≥λ2≥…≥λn.The maximum eigenvalueλ1 is called the spectral radius of G.In this paper,we characterize the extremal graphs that attain the maximum or minimum spectral radii among all graph complements in the family of graphs with cut vertices. 展开更多
关键词 spectral radius complements cut vertices
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Repetitive traumatic brain injury–induced complement C1–related inflammation impairs long-term hippocampal neurogenesis 认领 引用 被引量：4
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作者 Jing Wang Bing Zhang +9 位作者 Lanfang Li Xiaomei Tang Jinyu Zeng Yige Song Chao Xu Kai Zhao Guoqiang Liu Youming Lu Xinyan Li Kai Shu 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第3期821-835,共15页
Repetitive traumatic brain injury impacts adult neurogenesis in the hippocampal dentate gyrus,leading to long-term cognitive impairment.However,the mechanism underlying this neurogenesis impairment remains unknown.In ... Repetitive traumatic brain injury impacts adult neurogenesis in the hippocampal dentate gyrus,leading to long-term cognitive impairment.However,the mechanism underlying this neurogenesis impairment remains unknown.In this study,we established a male mouse model of repetitive traumatic brain injury and performed long-term evaluation of neurogenesis of the hippocampal dentate gyrus after repetitive traumatic brain injury.Our results showed that repetitive traumatic brain injury inhibited neural stem cell proliferation and development,delayed neuronal maturation,and reduced the complexity of neuronal dendrites and spines.Mice with repetitive traumatic brain injuryalso showed deficits in spatial memory retrieval.Moreover,following repetitive traumatic brain injury,neuroinflammation was enhanced in the neurogenesis microenvironment where C1q levels were increased,C1q binding protein levels were decreased,and canonical Wnt/β-catenin signaling was downregulated.An inhibitor of C1 reversed the long-term impairment of neurogenesis induced by repetitive traumatic brain injury and improved neurological function.These findings suggest that repetitive traumatic brain injury–induced C1-related inflammation impairs long-term neurogenesis in the dentate gyrus and contributes to spatial memory retrieval dysfunction. 展开更多
关键词 complement C1 dendrite dentate gyrus hippocampus neural stem cell neurogenesis neuroinflammation neurological function neuron traumatic brain injury
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Complement-dependent neuroinflammation in spinal cord injury:from pathology to therapeutic implications 认领 引用 被引量：2
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作者 Hassan Saad Bachar El Baba +10 位作者 Ali Tfaily Firas Kobeissy Juanmarco Gutierrez Gonzalez Daniel Refai Gerald R.Rodts Christian Mustroph David Gimbel Jonathan Grossberg Daniel L.Barrow Matthew F.Gary Ali M.Alawieh 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第5期1324-1335,共12页
Spinal cord injury remains a major cause of disability in young adults,and beyond acute decompression and rehabilitation,there are no pharmacological treatments to limit the progression of injury and optimize recovery... Spinal cord injury remains a major cause of disability in young adults,and beyond acute decompression and rehabilitation,there are no pharmacological treatments to limit the progression of injury and optimize recovery in this population.Following the thorough investigation of the complement system in triggering and propagating cerebral neuroinflammation,a similar role for complement in spinal neuroinflammation is a focus of ongoing research.In this work,we survey the current literature investigating the role of complement in spinal cord injury including the sources of complement proteins,triggers of complement activation,and role of effector functions in the pathology.We study relevant data demonstrating the different triggers of complement activation after spinal cord injury including direct binding to cellular debris,and or activation via antibody binding to damage-associated molecular patterns.Several effector functions of complement have been implicated in spinal cord injury,and we critically evaluate recent studies on the dual role of complement anaphylatoxins in spinal cord injury while emphasizing the lack of pathophysiological understanding of the role of opsonins in spinal cord injury.Following this pathophysiological review,we systematically review the different translational approaches used in preclinical models of spinal cord injury and discuss the challenges for future translation into human subjects.This review emphasizes the need for future studies to dissect the roles of different complement pathways in the pathology of spinal cord injury,to evaluate the phases of involvement of opsonins and anaphylatoxins,and to study the role of complement in white matter degeneration and regeneration using translational strategies to supplement genetic models. 展开更多
关键词 complement neuroinflammation neuroplasticity regeneration spinal cord injury targeted therapy
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Thyroid hormone,immunoglobin and complements for predicting hepatocellular carcinoma development in patients with hepatitis B virus-related liver cirrhosis 认领 引用
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作者 Xue-Cheng Tong Kai Liu +2 位作者 Ze-Yu Huang Xiu-Jun Zhang Yuan Xue 《World Journal of Hepatology》 2025年第2期130-139,共10页
BACKGROUND Hepatocellular carcinoma(HCC)surveillance is crucial for patients with compensated cirrhosis(CC)and decompensated cirrhosis(DC).Increasing evidence has revealed a connection between thyroid hormone(TH)and H... BACKGROUND Hepatocellular carcinoma(HCC)surveillance is crucial for patients with compensated cirrhosis(CC)and decompensated cirrhosis(DC).Increasing evidence has revealed a connection between thyroid hormone(TH)and HCC,although this relationship remains contentious.Complements and immunoglobulin(Ig),which serve as surrogates of cirrhosis-associated immune dysfunc-tion,are associated with the severity and outcomes of liver cirrhosis(LC).To date,there is a lack of evidence supporting the recommendation of TH,Ig,and com-plement tests in patients at high risk of HCC.AIM To assess the predictive value of TH,Ig,and complements for HCC development.METHODS Data from 142 patients,comprising 72 patients with CC and 70 patients with DC,were analysed as a training set.Among them,100 patients who underwent complement and Ig tests were considered for internal validation.Logistic regression was employed to identify independent risk factors for HCC development.RESULTS The median follow-up duration was 32(24-37 months)months.The incidence of HCC was significantly higher in the DC group(16/70,22.9%)compared to the CC group(3/72,4.2%)(χ2=10.698,P<0.01).Patients with DC exhibited lower total tetraiodothyronine(TT4),total triiodothyronine(TT3),free triiodothyronine,complement C3,and C4(all P<0.01),and higher IgA and IgG(both P<0.01).In both CC and DC patients,TT3 and TT4 positively correlated with alanine transaminase(ALT),aspartate transaminase(AST),and gamma-glutamyl transpeptidase(GGT).IgG positively correlated with IgM,IgA,ALT,and AST,while it negatively correlated with C3 and C4.Multivariable analysis indicated that age,DC status,and GGT were independent risk factors for HCC development.CONCLUSION The predictive value of TH,Ig,and complements for HCC development is suboptimal.Age,DC,and GGT emerge as more significant factors during HCC surveillance in hepatitis B virus-related LC. 展开更多
关键词 Thyroid hormone Immunoglobulin Complement Hepatocellular carcinoma Prediction
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A Machine-Learning Prognostic Model for Colorectal Cancer Using a Complement-Related Risk Signature 认领 引用
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作者 Jun Li Kangmin Yu +5 位作者 Zhiyong Chen Dan Xing Binshan Zha Wentao Xie Huan Ouyang Changjun Yu 《Oncology Research》 SCIE 2025年第11期3469-3492,共24页
Objectives:Colorectal cancer(CRC)remains a major contributor to global cancer mortality,ranking second worldwide for cancer-related deaths in 2022,and is characterized by marked heterogeneity in prognosis and therapeu... Objectives:Colorectal cancer(CRC)remains a major contributor to global cancer mortality,ranking second worldwide for cancer-related deaths in 2022,and is characterized by marked heterogeneity in prognosis and therapeutic response.We sought to construct a machine-learning prognosticmodel based on a complement-related risk signature(CRRS)and to situate this signature within the CRC immune microenvironment.Methods:Transcriptomic profiles with matched clinical annotations from TCGA and GEO CRC cohorts were analyzed.Prognostic CRRS genes were screened using Cox proportional hazards modeling alongside machine-learning procedures.A random survival forest(RSF)predictor was trained and externally validated.Comparisons of immune infiltration,mutational burden,pathway enrichment,and drug sensitivity were made between risk groups.The function of FAM84A,a key model gene,was examined in CRC cell lines.Results:The six-gene CRRS model accurately stratified patients by survival outcomes.Low-risk patients exhibited greater immune cell infiltration and higher predicted response to immunotherapy and chemotherapy,while high-risk patients showed enrichment of complement activation and matrix remodeling pathways.FAM84A was shown to promote CRC cell proliferation,migration,and epithelial–mesenchymal transition.Conclusion:CRRS is a critical modulator of the CRC immune microenvironment.The developed model enables precise risk prediction and supports individualized therapeutic decisions in CRC. 展开更多
关键词 Colorectal cancer complement response tumor microenvironment prognostic model the cancer genome atlas complement-related risk signature(CRRS)
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Incompressible Pairwise Incompressible Surfaces in Knot Complement 认领 引用
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作者 Youfa HAN Bingyu LUAN +1 位作者 Wenyue HOU Xintong WANG 《Journal of Mathematical Research with Applications》 CSCD 2025年第6期835-849,共15页
We deal with the properties of incompressible and pairwise incompressible surfaces in knot complements through the application of relevant properties of almost simple topological graphs.We analyze the topological grap... We deal with the properties of incompressible and pairwise incompressible surfaces in knot complements through the application of relevant properties of almost simple topological graphs.We analyze the topological graph invariants associated with surfaces embedded in the complements of alternating and almost alternating knots.Specifically,we prove that the characteristic numbers of these graphs remain invariant under two fundamental transformations(R-move and S2-move).Leveraging the interplay between characteristic numbers and Euler characteristics,and further connecting Euler characteristics to surface genus,we derive novel results regarding the genus of incompressible pairwise incompressible surfaces.Additionally,we establish a discriminant criterion to determine when such surfaces in knot complements admit genus zero. 展开更多
关键词 topological graph almost simple topological graphs knot complement incompressible surface pairwise incompressible surface
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Research progress on the roles of complement in liver injury 认领 引用
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作者 Li-Li Ou Jin-Lian Jiang +3 位作者 Man-Lu Guo Jin-Hua Wu Wei-Wei Zhong Yi-Huai He 《World Journal of Hepatology》 2025年第3期13-24,共12页
The complement system is crucial for maintaining immunological homeostasis in the liver,playing a significant role in both innate and adaptive immune responses.Dysregulation of this system is closely linked to the pat... The complement system is crucial for maintaining immunological homeostasis in the liver,playing a significant role in both innate and adaptive immune responses.Dysregulation of this system is closely linked to the pathogenesis of various liver diseases.Modulating the complement system can affect the progression of these conditions.To provide insights into treating liver injury by targeting the regu-lation of the complement system,we conducted a comprehensive search of major biomedical databases,including MEDLINE,PubMed,EMBASE,and Web of Science,to identify articles on complement and liver injury and reviewed the functions and mechanisms of the complement system in liver injury. 展开更多
关键词 Complement system Liver injury Immune homeostasis Pathogenesis Review
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Critical role of complement in antibody mediated rejection in kidney transplantation 认领 引用
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作者 Khawar Abbas Muhammed Mubarak +2 位作者 Wajiha Musharraf Tahir Aziz Mirza Naqi Zafar 《World Journal of Transplantation》 2025年第4期157-171,共15页
Antibody-mediated rejection(AMR)represents a major challenge in kidney transplantation,significantly contributing to tissue injury and graft failure.AMR is primarily driven by donor-specific alloantibodies(DSAs),which... Antibody-mediated rejection(AMR)represents a major challenge in kidney transplantation,significantly contributing to tissue injury and graft failure.AMR is primarily driven by donor-specific alloantibodies(DSAs),which recognize and bind to specific target antigens present within the transplanted kidney tissue.Upon binding,these DSAs commonly initiate activation of the complement system within the graft.The activation of the complement cascade sets off a powerful inflammatory response characterized by the recruitment and activation of immune cells,endothelial damage,and subsequent tissue injury.This inflammation underlies many clinical and histological manifestations of AMR,making complement activation a critical player in the disease process.Advancements in our understanding of how complement pathways contribute to kidney graft injury have opened new avenues for therapeutic intervention.Recent research has facilitated the development and application of novel therapies specifically designed to inhibit complement activation.Such targeted complement-inhibitory strategies have shown promise in improving graft outcomes by inhibiting complement-mediated damage and extending graft survival.This review comprehensively discusses the critical role of complement activation in inducing kidney graft injury with a focus on its role in AMR.By elucidating the detailed mechanisms and contributions of complement pathways,the review seeks to enhance the understanding necessary for developing targeted therapeutic interventions to prevent or treat AMR effectively. 展开更多
关键词 Complement Donor-specific antibodies Kidney Allograft Rejection Graft failure
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EREG-secreting THBS1+tissue monocytes are recruited by C5a to promote rapid liver regeneration in patients and mice during the ALPPS procedure 认领 引用 被引量：1
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作者 Feiyu Chen Jiayan Yan +12 位作者 Zhifeng Jiang Jianwen Cheng Na Yao Ao Huang Shiyu Zhang Yang Xu Haixiang Sun Zheng Wang Zhaoyou Tang Xiangdong Wang Jia Fan Xinrong Yang Jian Zhou 《Hepatobiliary Surgery and Nutrition》 SCIE 2026年第2期25-46,共22页
Background:Associating liver partition and portal vein ligation for staged hepatectomy(ALPPS)is an important surgical treatment for unresectable liver tumors,while with its mechanism remaining unclear.We aim to compre... Background:Associating liver partition and portal vein ligation for staged hepatectomy(ALPPS)is an important surgical treatment for unresectable liver tumors,while with its mechanism remaining unclear.We aim to comprehensively examine the key immune cells that induce the rapid liver regeneration during the ALPPS procedure and unearth the relevant mechanism(s)in patients with hepatocellular carcinoma(HCC).Methods:Matched ALPPS stage Ⅰ and Ⅱ liver tissues were collected from five HCC patients and subjected to cytometry by time-of-flight(CyTOF)and single-cell RNA sequencing(scRNA-seq)analysis.Peripheral blood samples were collected during subsequent routine clinical examinations to explore the dynamic changes in circulating immune cells and cytokines.The changes in the transcription profiles of liver tissues between ALPPS stage Ⅰ and Ⅱ were explored by bulk RNA-seq analysis.Tissue microarrays containing paired tissues from another 22 HCC patients who underwent ALPPS were constructed for validation.Results:The CyTOF data revealed an increase in tissue monocytes during the ALPPS-induced liver regeneration(from 13.36%to 29.78%,P=0.04).There was also a shift from a macrophage-enriched to monocyte-enriched local immune environment in the remnant liver tissues induced by ALPPS.The scRNA-seq analysis identified that a cluster of THBS1+tissue monocytes was significantly enriched in the regenerated liver tissues in all three patients,with high expression of epiregulin(EREG).Further analysis indicated that THBS1+tissue monocytes promote hepatocyte proliferation via EREG-epidermal growth factor receptor(EGFR)interactions.The secretion of C5a by hepatocytes could recruit THBS1+tissue monocytes via the C5a/C5aR1 interaction.The functions of EREG and C5a have been verified in vitro and in vivo.Conclusions:The ALPPS procedure induced activation of the complement system in hepatocytes,specifically increasing the expression of C5a,which led to the recruitment of THBS1+tissue monocytes through the C5a/C5aR1 interaction.These monocytes then secrete EREG to promote hepatocyte proliferation in the residual liver. 展开更多
关键词 Liver regeneration associating liver partition and portal vein ligation for staged hepatectomy(ALPPS) monocyte complement
融合柔性养殖负荷与储能的高光伏渗透率渔光台区运行策略 认领 引用 被引量：1
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作者 田志曈 张轶炫 +3 位作者 刘谋海 马叶钦 刘晓川 鲁海亮 《电力系统自动化》 EI CSCD 北大核心 2026年第7期193-205,共13页
在“双碳”目标与各类政策驱动下,农村分布式光伏装机容量快速增长,大规模光伏接入导致中国南方大量渔光互补台区出现严重的反向过载。与此同时,渔塘养殖负荷因其可预测性与可调节性,展现出显著的柔性潜力。为此,文中面向高光伏渗透率... 在“双碳”目标与各类政策驱动下,农村分布式光伏装机容量快速增长,大规模光伏接入导致中国南方大量渔光互补台区出现严重的反向过载。与此同时,渔塘养殖负荷因其可预测性与可调节性,展现出显著的柔性潜力。为此,文中面向高光伏渗透率渔光台区,提出一种基于柔性养殖负荷与储能协同的反向过载治理策略。首先,基于实际台区全年运行数据,提取最严重光伏出力工况并构建净负荷曲线,从而揭示反向过载的典型特性;然后,从鱼类需氧机理与增氧机耦合特性出发,构建单机氧含量演化的微分动力学模型,进而推导夜间供氧负荷的不可调特性,并量化喂食增氧与晴天补氧负荷的可平移与可转移能力以及需求响应比例;在此基础上,构建柔性负荷与储能的协同优化模型,以避免反向功率越限并提升光伏消纳能力;最后,在改进的IEEE 33节点渔光台区等不同拓扑系统上开展算例验证。结果表明,所提策略能够有效消除反向过载、显著降低运行成本,并在不同规模台区均保持较好的适用性与经济性。 展开更多
关键词 光伏 台区 反向过载 增氧机 渔光互补 养殖负荷 储能 需求响应
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