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Roles of central nervous system resident and recruited macrophages in the brain barrier system 认领 引用
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作者 Ze Liu Teng Cheng +5 位作者 Hongtian Dong Dingya Sun Yan Wang Jiayan Li Zhongwang Yu Li Cao 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第3期855-868,共14页
Macrophages in the brain barrier system include microglia in the brain parenchyma,border-associated macrophages at the brain’s borders,and recruited macrophages.They are responsible for neural development,maintenance... Macrophages in the brain barrier system include microglia in the brain parenchyma,border-associated macrophages at the brain’s borders,and recruited macrophages.They are responsible for neural development,maintenance of homeostasis,and orchestrating immune responses.With the rapid exploitation and development of new technologies,there is a deeper understanding of macrophages in the brain barrier system.Here we review the origin,development,important molecules,and functions of macrophages,mainly focusing on microglia and border-associated macrophages.We also highlight some advances in single-cell sequencing and significant cell markers.We anticipate that more advanced methods will emerge to study resident and recruited macrophages in the future,opening new horizons for neuroimmunology and related peripheral immune fields. 展开更多
关键词 border-associated macrophages brain barrier system cell markers development microglia neuroimmunology recruited macrophages resident macrophages single-cell sequencing
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Changes in border-associated macrophages after stroke: Single-cell sequencing analysis 认领 引用 被引量：2
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作者 Ning Yu Yang Zhao +3 位作者 Peng Wang Fuqiang Zhang Cuili Wen Shilei Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第1期346-356,共11页
Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macro... Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macrophages have been poorly understood and largely overlooked. However, a recent study reported that border-associated macrophages participate in stroke-induced inflammation, although many details and the underlying mechanisms remain unclear. In this study, we performed a comprehensive single-cell analysis of mouse border-associated macrophages using sequencing data obtained from the Gene Expression Omnibus(GEO) database(GSE174574 and GSE225948). Differentially expressed genes were identified, and enrichment analysis was performed to identify the transcription profile of border-associated macrophages. CellChat analysis was conducted to determine the cell communication network of border-associated macrophages. Transcription factors were predicted using the ‘pySCENIC' tool. We found that, in response to hypoxia, borderassociated macrophages underwent dynamic transcriptional changes and participated in the regulation of inflammatory-related pathways. Notably, the tumor necrosis factor pathway was activated by border-associated macrophages following ischemic stroke. The pySCENIC analysis indicated that the activity of signal transducer and activator of transcription 3(Stat3) was obviously upregulated in stroke, suggesting that Stat3 inhibition may be a promising strategy for treating border-associated macrophages-induced neuroinflammation. Finally, we constructed an animal model to investigate the effects of border-associated macrophages depletion following a stroke. Treatment with liposomes containing clodronate significantly reduced infarct volume in the animals and improved neurological scores compared with untreated animals. Taken together, our results demonstrate comprehensive changes in border-associated macrophages following a stroke, providing a theoretical basis for targeting border-associated macrophages-induced neuroinflammation in stroke treatment. 展开更多
关键词 border-associated macrophages clodronate hypoxia ischemia-reperfusion ischemic stroke liposomes neuroinflammation single-cell sequencing analysis STAT3 tumor necrosis factor
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Macrophages-derived NRG-1 promotes angiogenesis after ischemic stroke via the Akt-mTOR pathway 认领 引用 被引量：1
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作者 Jie Chen Bo Wang +4 位作者 Danyang Fan Xi Chen Lenv Gao Yun Luo Zhenhua Zhou 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3007-3016,共10页
Acute ischemic stroke remains a significant health concern owing to the limited efficacy of current therapeutic options.In recent years,Neuregulin-1 has exhibited promising neuroprotective effects in cerebral ischemia... Acute ischemic stroke remains a significant health concern owing to the limited efficacy of current therapeutic options.In recent years,Neuregulin-1 has exhibited promising neuroprotective effects in cerebral ischemia.However,the sources and functions of Neuregulin-1 have not yet been fully understood,which hinders its translation and broad application.Here,we collected paired clot and peripheral blood samples from patients with acute ischemic stroke to determine the sources of Neuregulin-1.In addition,we established an in vivo transient middle cerebral artery occlusion mouse model to investigate the therapeutic effects of Neuregulin-1 and its underlying molecular biological mechanisms.We observed a significant elevation in serum Neuregulin-1 levels among patients with acute ischemic stroke that correlated with severity of neurological impairment and clinical outcome.Using single-cell sequencing,we identified Neuregulin-1-positive macrophages among peripheral blood mononuclear cells that produced Neuregulin-1 post-ischemia.In addition,Neuregulin-1 promoted repair of the infarcted area,alleviating neuronal and myelin damage and improving overall behavioral recovery in mice.We found that Neuregulin-1 may exert these neuroprotective effects by promoting angiogenesis in the infarct area,and that this effect is mediated by Akt/mTOR/VEGF-dependent signaling.Our findings suggest that peripheral macrophages are a source of Neuregulin-1 post-stroke.Neuregulin-1 exerts its neuroprotective effects by promoting angiogenesis via Akt/mTOR/VEGF-dependent signaling,showing promising clinical translation potential. 展开更多
关键词 acute ischemic stroke angiogenesis Clot ErbB4 fluorescence-activated cell sorting immune cell inflammation macrophages Neuregulin-1 neuroprotection
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Targeting Inflammaging:A Metformin-Releasing Titanium Implant Reprograms Senescent Macrophages to Orchestrate Angiogenesis and Osteogenesis 认领 引用
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作者 Ruiyue Hang Ruoyu Di +4 位作者 Yuyu Zhao Jiahui Wang Xiaohong Yao Ruiqiang Hang Yin Xiao 《Rare Metals》 SCIE EI CAS CSCD 2026年第7期644-661,共18页
Bone defect repair in elderly patients is frequently compromised by reduced osteogenic capacity and delayed healing.Chronic inflammation-driven inflammaging is a critical contributor to this impairment,characterized b... Bone defect repair in elderly patients is frequently compromised by reduced osteogenic capacity and delayed healing.Chronic inflammation-driven inflammaging is a critical contributor to this impairment,characterized by dysfunctional autophagy in senescent macrophages(S-MΦs),excessive reactive oxygen species(ROS)accumulation,and persistent proinflammatory M1 polarization.These factors ultimately disrupt the essential coupling between angiogenesis and osteogenesis.Herein,we investigated whether metformin-mediated autophagy induction could restore intracellular homeostasis in S-MΦs to reestablish a regenerative osteoimmune microenvironment.To achieve this locally,we engineered a titanium(Ti)-based coating system for sustained metformin delivery.We found that 0.1 mM metformin restored S-MΦhomeostasis by enhancing autophagy(about 1-fold higher autophagosome fluorescence)and reducing oxidative stress(about 50%lower ROS),thereby promoting prohealing M2 polarization,with about 40%higher CD206 and 70%lower iNOS expression.Consequently,the microenvironment modulated by rejuvenated S-MΦs significantly alleviated oxidative stress in senescent endothelial cells(S-ECs)and osteoblasts(S-OBs),recovering their angiogenic and osteogenic functions.Material-wise ordered titanium dioxide nanotubes(TNTs)were functionalized with layer-by-layer polydopamine(PDA)to enable efficient metformin loading and controlled release.This functionalized surface supported S-MΦviability and favorable morphology.Current mechanistic validation via exogenous stimulation and conditioned media,combined with the coating’s controllable drug release and biocompatibility,offers a promising strategy to enhance Ti implant integration in the context of aging-associated immune dysfunction. 展开更多
关键词 angiogenesis metformin osteogenesis senescent macrophages titanium dioxide nanotubes
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Differential metabolites facilitate metabolic dysfunction-associated fatty liver disease malignancy via immune evasion and M2-polarized macrophages 认领 引用
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作者 Jie Yang Wen-Li Sai +5 位作者 Xiao-Xiao Xia Hao Tang Min Xu Qun Xie Deng-Fu Yao Min Yao 《World Journal of Gastroenterology》 SCIE CAS 2026年第24期97-116,共20页
BACKGROUND Differential metabolites(DMs)are associated with metabolic dysfunction-associated fatty liver disease(MAFLD)malignant transformation.However,their underlying mechanisms remain to be identified.AIM To invest... BACKGROUND Differential metabolites(DMs)are associated with metabolic dysfunction-associated fatty liver disease(MAFLD)malignant transformation.However,their underlying mechanisms remain to be identified.AIM To investigate the dynamic alterations of DMs,carnitine palmitoyl transferase-II(CPT-II)and immune cells during MAFLD malignancy.METHODS A rat model was constructed with high fat diet plus 2-fluorenylacetamide to induce hepatocyte malignancy.Livers were divided into MAFLD,metabolic dysfunction-associated steatohepatitis,liver cirrhosis(LC)and hepatocellular carcinoma(HCC)groups based on hematoxylin and eosin staining,with normal rats as control.DMs were identified via RNA transcriptomics or metabolomics.Proteins were detected by western blotting,and immune cells were analyzed by single-cell sequencing.RESULTS Model livers with obvious lipid accumulation and cells were examined during MAFLD malignancy from inflammation or necrosis to LC or HCC and exhibited a pathological alteration of nuclear pleomorphism,disordered arrangement and a progressive decrease in CPT-II activity.The number of DMs was 131 in MAFLD,134 in metabolic dysfunction-associated steatohepatitis,27 in liver fibrosis/LC,and 130 in HCC,respectively.Cyclin B1 and cyclin-dependent kinase 1 were involved in the P53 pathway and cell cycle,and they held key positions in the protein interaction network,which involved metabolic regulation of cell response to stimuli.DMs,such as phosphatidylcholine or sphingomyelin in steroid biosynthesis,were significantly related to MAFLD malignancy.Mechanistically,liver immune cells undergo dynamic changes in a fat-rich microenvironment,with decreased T cell abundance and increased programmed death ligand 1 expression and M2-polarized macrophages.CONCLUSION Downregulated CPT-II aggravates the accumulation of metabolites associated with MAFLD malignancy via immune evasion and M2-polarized macrophages. 展开更多
关键词 Differential metabolites Carnitine palmitoyl transferase-II Immune escape Differentially expressed genes M2-polarized macrophages Hepatocarcinogenesis
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Targeting macrophages in OA nanomedicine:Therapeutic opportunity or delivery delusion? A pragmatic reappraisal 认领 引用
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作者 Qing Yao Beilin Fu Longfa Kou 《Asian Journal of Pharmaceutical Sciences》 SCIE CAS CSCD 2026年第1期1-3,共3页
1. Introduction Osteoarthritis(OA), traditionally viewed as a mechanical and degenerative condition, increasingly involves chronic,low-grade inflammation. Among implicated immune cells,activated macrophages are key dr... 1. Introduction Osteoarthritis(OA), traditionally viewed as a mechanical and degenerative condition, increasingly involves chronic,low-grade inflammation. Among implicated immune cells,activated macrophages are key drivers of synovitis and cartilage degradation [1], spurring interest in therapies that selectively modulate macrophage activity within the joint while sparing other resident cells. 展开更多
关键词 macrophages osteoarthritis inflammation nanomedicine therapeutic opportunity delivery strategy
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Growth differentiation factor 11 reprograms M2-like macrophages:Targeting immunometabolism for cancer therapy 认领 引用
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作者 Saeed Mohammadi Mahmoud Darweesh Ahmed Al-Harrasi 《World Journal of Gastroenterology》 SCIE CAS 2026年第10期1-7,共7页
This editorial comments on recent research by Escobedo-Calvario et al.Their study revealed that growth differentiation factor 11(GDF11)functions as a potent,non-cytotoxic immunometabolic modulator within the tumor mic... This editorial comments on recent research by Escobedo-Calvario et al.Their study revealed that growth differentiation factor 11(GDF11)functions as a potent,non-cytotoxic immunometabolic modulator within the tumor microenvironment.GDF11 treatment initiates an intense reprogramming in pro-tumoral M2-like macrophages by activating the Smad2/3 pathway and driving a fundamental shift in cellular identity.This reversal is highlighted by the significant downregulation of the M2 marker cluster of differentiation 206 and critical metabolic restructuring,including enhanced mitochondrial function(increased oxygen consumption rate),decreased total cellular cholesterol content,and a necessary increase in reactive oxygen species production.This work uniquely positions GDF11 as a dual-axis therapeutic agent,capable of both direct tumor inhibition and immunometabolic reprogramming of M2-like macrophages,yielding a re-educated secretome that effectively suppresses the pro-proliferative and migratory capacity of hepatocellular carcinoma cells.It suggests GDF11 may be a promising,mechanism-based therapeutic strategy for simultaneously managing the progression of a subset of malignancies and resolving the underlying chronic inflammatory and metabolic disorders associated with M2-like macrophage dysfunction. 展开更多
关键词 Growth differentiation factor 11 Macrophages Immunometabolism Macrophage polarization Cancer Tumor microenvironment Hepatocellular carcinoma
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Polysialic acid-Siglec immune checkpoints of microglia and macrophages:Perspectives for therapeutic intervention 认领 引用
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作者 Hauke Thiesler Herbert Hildebrandt 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第2期661-662,共2页
Microglia are the resident macrophages of the central nervous system.They act as the first line of defense against pathogens and play essential roles in neuroinflammation and tissue repair after brain insult or in neu... Microglia are the resident macrophages of the central nervous system.They act as the first line of defense against pathogens and play essential roles in neuroinflammation and tissue repair after brain insult or in neurodegenerative and demyelinating diseases(Borst et al.,2021).Together with infiltrating monocyte-derived macrophages,microglia also play a critical role for brain tumor development,since immunosuppressive interactions between tumor cells and tumor-associated microglia and macrophages(TAM)are linked to malignant progression.This mechanism is of particular relevance in glioblastoma(GB),the deadliest form of brain cancer with a median overall survival of less than 15 months(Khan et al.,2023).Therefore,targeting microglia and macrophage activation is a promising strategy for therapeutic interference in brain disease. 展开更多
关键词 therapeutic intervention central nervous system immune checkpoints neurodegenerative demyelinating diseases borst macrophages polysialic acid Siglec microglia
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Molecular mechanisms of tumor-associated macrophages in hepatocellular carcinoma development and therapy 认领 引用
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作者 Ming Yang Chun-Ye Zhang 《World Journal of Gastroenterology》 SCIE CAS 2026年第8期31-43,共13页
Hepatocellular carcinoma(HCC)is the most common type of primary liver cancer and ranks as the sixth most common cancer and the third leading cause of cancerrelated death worldwide.Tumor-associated macrophages(TAMs)are... Hepatocellular carcinoma(HCC)is the most common type of primary liver cancer and ranks as the sixth most common cancer and the third leading cause of cancerrelated death worldwide.Tumor-associated macrophages(TAMs)are predominant immune cells in the tumor microenvironment of HCC,playing critical roles in cancer cell proliferation,epithelial-mesenchymal transition,and metastasis.Reprogramming TAMs from a pro-tumoral phenotype to an anti-tumoral phenotype can enhance macrophage-mediated phagocytosis of HCC cells,improve cytotoxic T cell function,and increase the efficacy of immunotherapies.In this review,we summarize recent findings on how TAMs contribute to HCC development and progression,examine molecular markers and important signaling pathways that regulate TAM function within the tumor microenvironment,and discuss strategies for targeting TAMs at the cellular and molecular levels to treat HCC. 展开更多
关键词 Hepatocellular carcinoma Macrophages Immune checkpoint inhibitors Immunotherapy Signaling pathways
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Distribution and prognostic value of macrophages in colorectal cancer and adjacent mucosa in patient stagesⅠ-ⅢvsⅣ 认领 引用 被引量：1
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作者 Wen-Jing Ye Esraa Ali +9 位作者 Sergii Pavlov Lenka Cervenková Filip Ambrozkiewicz Ondřej Vyčítal Petr Hošek František Zitrický Ondřej Daum Václav Liška Kari Hemminki Andriy Trailin 《World Journal of Gastroenterology》 SCIE CAS 2026年第10期52-66,共15页
BACKGROUND Synchronous and metachronous liver metastases(LM)of colorectal cancer(CRC)drastically worsen the patient’s survival.The biological and immunological mechanisms underlying these distinct metastatic trajecto... BACKGROUND Synchronous and metachronous liver metastases(LM)of colorectal cancer(CRC)drastically worsen the patient’s survival.The biological and immunological mechanisms underlying these distinct metastatic trajectories remain incompletely understood.Prognostic impact of macrophages in primary CRC(pCRC)is uncertain,with discrepant findings reported for different macrophage subsets and different stage of the disease.Most of prior studies of tumor-infiltrating macrophages in CRC have focused primarily on the tumor core or invasive margin,whereas less attention has been given to the adjacent nontumor mucosa(NM),which may harbor early immunological alterations that precede or accompany metastatic spread.AIM To evaluate distribution and prognostic value of macrophages in pCRC and NM in patients at stage Ⅰ-Ⅲ vs Ⅳ.METHODS Paired specimens of pCRC and NM were collected retrospectively from:(1)Stage Ⅳ(n=55)patients with synchronous LM;and(2)Stage Ⅰ-Ⅲ(n=44)patients who developed metachronous LM thereafter.After immunohistochemical staining CD68+(M0),CD80+(M1),CD206+and CD163+(M2)macrophages were quantified in NM and tumor center(TC)of pCRC.Cell densities in NM and TC and TC/NM ratios were tested as prognostic variables for overall survival since liver surgery.Cox-regression and Kaplan-Meier analyses were applied using the R environment.RESULTS Densities of macrophages followed the declining pattern from CD163+through CD206+and CD68+to CD80+in both NM and TC,with significantly smaller densities of all cell types in tumors.Greater densities of CD80+cells were observed in NM in stage I-Ⅲ over stage Ⅳ patients:309(24-1143)cells/mm2 vs 208(3-1084)cells/mm2[median(minimum-maximum),P=0.04].High CD163+cell density in NM in stage Ⅳ[hazard ratio=0.45(95%CI:0.22-0.95),P=0.04]and CD80+cell density in NM in stage Ⅰ-Ⅲ[hazard ratio=0.24(95%CI:0.10-0.57),P=0.001]were associated with longer overall survival.CONCLUSION Contrary to TC of pCRC,we found favorable prognostic implications of macrophages in NM,driven by distinct subsets of macrophages in stage Ⅳ(CD163+M2)and stage Ⅰ-Ⅲ CRC(CD80+M1). 展开更多
关键词 Macrophages Primary colorectal cancer Adjacent nontumor mucosa Liver metastases Survival
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Tumor-associated macrophages in hepatocellular carcinoma:Cellular plasticity and therapy resistance in crosstalk 认领 引用 被引量：1
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作者 Tianhao Zhang Xi Zhao +1 位作者 Tingting Gao Fang Ma 《Journal of Pharmaceutical Analysis》 SCIE CAS CSCD 2026年第1期5-16,共12页
Hepatocellular carcinoma(HCC)is the predominant type of liver cancer.There are different risk factors for HCC including viral infection,liver fibrosis,non-alcoholic fatty liver disease,environmental factors and genomi... Hepatocellular carcinoma(HCC)is the predominant type of liver cancer.There are different risk factors for HCC including viral infection,liver fibrosis,non-alcoholic fatty liver disease,environmental factors and genomic alterations.The tumor microenvironment(TME)has been proposed as a potent regulator of tumor malignancy comprised of normal and cancerous cells.Macrophages are among the most abundant cells in the TME,known as tumor-associated macrophages(TAMs)that can control proliferation,metastasis,immune reactions and therapy response of tumor cells.In the present review,the function of TAMs in the regulation of HCC progression was evaluated.TAMs are prognostic factors in HCC that increase in TAM infiltration into TME can cause undesirable outcome in patients.Moreover,M2 polarization of macrophages can impair function of other immune cells such as T cells and natural killer(NK)cells to mediate immune evasion.TAMs demonstrate association with other biological events including autophagy and glycolysis.There is mutual interaction between TAMs and exosomes that TAM-mediated exosome secretion regulates HCC progression,while exosomes derived from other cells can also affect TAMs.Inhibition of macrophage recruitment,their depletion and increasing M1 polarization are promising approaches in HCC therapy.The natural products and nanostructures have been also recently introduced for the regulation of macrophages in HCC therapy. 展开更多
关键词 Hepatocellular carcinoma Immunotherapy Tumor microenvironment Tumor-associated macrophages Drug delivery
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Effects and mechanism of Bifidobacterium on intestinal inflammation resulting from deoxycholic acid-induced M1 polarization of macrophages 认领 引用 被引量：2
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作者 Peng-Chun Yang Chun-Yan Xiao +6 位作者 Jing Wang Cai-Hua Yan Qi-Yi Li Shi-Yu Li Jian Li Li-Jing Zhang Chi-Bing Dai 《World Journal of Gastroenterology》 SCIE CAS 2026年第6期77-96,共20页
BACKGROUND A high-fat diet(HFD)can cause systemic low-grade inflammation,metabolic and inflammatory diseases,and alter the composition of intestinal microbiota.Although probiotics mitigate intestinal inflammation,it i... BACKGROUND A high-fat diet(HFD)can cause systemic low-grade inflammation,metabolic and inflammatory diseases,and alter the composition of intestinal microbiota.Although probiotics mitigate intestinal inflammation,it is still unclear whether they can directly inhibit the production of deoxycholic acid(DCA)to prevent or alleviate intestinal inflammation.AIM To investigate changes in intestinal flora,fecal DCA levels,and cytokine profiles.METHODS Vancomycin was administered to significantly reduce the population of intestinal gram-positive bacteria,which helped in reducing the fecal DCA levels.Recruitment of pro-inflammatory macrophages,polarization of macrophages,and the inflammation associated with the intestinal flora of the HFD animal model were assessed.Their expression levels were analyzed through real-time polymerase chain reaction,immunofluorescence staining,liquid chromatography-mass spectrometry,and 16S rRNA high-throughput sequencing.RESULTS HFD or DCA promotes the infiltration of colon macrophages,causing their polarization toward the M1 phenotype.This polarization can be inhibited by both vancomycin and Bifidoba-cterium.Bifidobacterium enhances the species richness and uniformity of the intestinal microbiota in HFD mice;however,it does not improve these parameters in the presence of vancomycin.Bifidobacterium also does not increase the abundance of microbiota in HFD-fed or HFD-and-vancomycin-treated mice.HFD alters the relative abundance of intestinal microbiota at the phylum and genus levels.Bifidobacterium or vancomycin can partially mitigate these changes.CONCLUSION Bifidobacterium can inhibit HFD-induced intestinal inflammation or that resulting from DCA-induced M1 polarization of macrophages.It may also regulate bile acid levels and target cholesterol metabolism pathways,which may serve as potential therapeutic strategies for HFD-associated colitis. 展开更多
关键词 High-fat diet Bifidobacterium Deoxycholic acid Macrophage polarization Microbiota Intestinal inflammation
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Ishige okamurae extract suppresses osteoclastogenesis in RANKL-induced bone marrow-derived macrophages and ovariectomized mouse model 认领 引用
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作者 Su-Hyeon Cho Hye-Yeon Jung +3 位作者 Songrae Kim You-Jee Jang Jae-Il Park Kil-Nam Kim 《Asian Pacific Journal of Tropical Biomedicine》 SCIE CAS 2026年第8期354-362,共9页
Objective:To investigate the inhibitory effects of Ishige okamurae extract(IOE)against osteoclastogenesis in vitro and in vivo.Methods:The effects of IOE on osteoclast differentiation were examined in receptor activat... Objective:To investigate the inhibitory effects of Ishige okamurae extract(IOE)against osteoclastogenesis in vitro and in vivo.Methods:The effects of IOE on osteoclast differentiation were examined in receptor activator of nuclear factor-κB ligand(RANKL)-stimulated bone marrow macrophages.Cell viability was examined using an MTT assay,while osteoclast formation and differentiation were determined by tartrate-resistant acid phosphatase(TRAP)staining kit.Protein expression levels of osteoclast-related factors,transcriptional factors,and signaling molecules involved in osteoclastogenesis were analyzed by Western blotting.The effect of IOE was examined in the ovariectomy(OVX)mouse model following oral administration,and osteoclast-related parameters were analyzed using 3D X-ray microscopy.Results:IOE significantly reduced RANKL-induced osteoclast formation and differentiation without causing cytotoxic effects on bone marrow macrophages.It suppressed the formation of TRAP-positive multinuclear osteoclasts and downregulated the expression of osteoclastrelated factors,such as TRAP(ACP5),matrix metalloproteinase-9,calcitonin receptor,and cathepsin K.Furthermore,IOE significantly inhibited the expression of key transcriptional factors,such as nuclear factor of activated T cells,cytoplasmic 1,and c-Fos.Mechanistically,IOE attenuated the activation of upstream extracellular signal-regulated kinase(ERK),c-Jun N-terminal kinase(JNK),and nuclear factor-κB(NF-κB)cascades.In OVX mice,administration of IOE significantly improved bone microstructural parameters such as trabecular thickness,number,volume,and separation.Conclusions:The present findings demonstrate that IOE inhibits osteoclastogenesis via blockage of ERK,JNK,and NF-κB signaling pathways in vitro.Furthermore,IOE administration reduces bone loss in OVX mice.These results show that IOE has the potential to be a functional food for the prevention of osteoporosis. 展开更多
关键词 Ishige okamurae Bone marrow macrophages Osteoclasts Ovariectomy 3D X-ray microscopy Mice JNK ERK NF-κB
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Pien Tze Huang exerts anti-tumor effect by promoting CSF-1R degradation and cleavage in tumor-associated macrophages 认领 引用
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作者 Jun-Jie Zhang Han-Shi Guo +5 位作者 Jing-Na Yuan Si-Yu Chen Bei Li Shi-Cong Wang Chun-Dong Yu Yi-Lin Hong 《Traditional Medicine Research》 2026年第11期14-26,共13页
Background:This study aimed to investigate the antitumor efficacy of Pien Tze Huang(PZH)in colorectal cancer(CRC)and elucidate its immunomodulatory mechanism,with a focus on tumor-associated macrophages(TAMs)and colon... Background:This study aimed to investigate the antitumor efficacy of Pien Tze Huang(PZH)in colorectal cancer(CRC)and elucidate its immunomodulatory mechanism,with a focus on tumor-associated macrophages(TAMs)and colony-stimulating factor 1 receptor(CSF-1R)signaling.Methods:Antitumor effects were evaluated in subcutaneous MC38 allograft and azoxymethane/dextran sulfate sodium(AOM/DSS)-induced CRC mouse models.TAMs infiltration was analyzed via immunohistochemistry and flow cytometry.Macrophage proliferation and migration were assessed by using MTT and Transwell assays.RNA sequencing,RT-qPCR,Western blotting,cycloheximide chase,inhibitor,polysome profiling,and gene silencing assays were performed to determine the mechanism underlying CSF-1R regulation.Results:PZH suppressed mouse CRC growth in both subcutaneous MC38 allograft and AOM/DSS-induced models,with its efficacy being partly dependent on reducing TAMs infiltration.In vitro assays further revealed that PZH impaired macrophage proliferation and migration.Mechanistically,PZH selectively downregulated CSF-1R via a multilayered program involving rapid posttranslational degradation through proteasomal and lysosomal pathways,as well as receptor proteolytic cleavage mediated by the TLR2-iRhom2-ADAM17 axis.Conclusion:Our experiments identify TAMs and CSF-1R as key cellular and molecular targets of PZH,thereby highlighting its ability to modulate TAMs within the tumor microenvironment(TME)and inhibit CRC progression.These results provide mechanistic insights into the immunomodulatory actions of PZH and identify CSF-1R as a promising target for macrophage-targeted therapies in CRC. 展开更多
关键词 Pien Tze Huang colorectal cancer tumor-associated macrophages CSF-1R TLR2-iRhom2-ADAM17 immunotherapy
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UCP2 Identifies Immunosuppressive Tumor-Associated Macrophages and Is Associated with Predicted Immunotherapy Resistance in Glioma 认领 引用
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作者 Hui Zhou Jiarui Wang +1 位作者 Zhili Qiao Xin Liao 《Oncology Research》 SCIE 2026年第8期471-497,共27页
Objectives:Uncoupling protein 2(UCP2)has been extensively studied as a metabolic regulator in glioma;however,its relationship with the tumour immune microenvironment and the cellular source of its expression within th... Objectives:Uncoupling protein 2(UCP2)has been extensively studied as a metabolic regulator in glioma;however,its relationship with the tumour immune microenvironment and the cellular source of its expression within the glioma tumour microenvironment(TME)remains poorly understood.This study aimed to characterise UCP2 expression at single-cell resolution and evaluate its immunological significance in glioma.Methods:This study employed an integrative multi-omics approach incorporating bulk transcriptomics,scRNA-seq(GSE70630,GSE84465,and GSE89567;n=13,216 cells),immune deconvolution,immunohistochemistry(n=96 glioma patients),and immunofluorescence co-staining(n=6).Results:Pan-cancer analysis confirmed UCP2 overexpression in glioma.Single-cell analysis revealed UCP2 expression within the TME is predominantly enriched in macrophage/microglial populations rather than tumour cells,reframing UCP2 as a tumour-associated macrophage(TAM)-intrinsic regulator.In the TCGA cohort(n=670),UCP2-high tumours exhibited an immunosuppressive landscape enriched with M2 macrophages and regulatory T cells,with elevated ESTIMATE scores.UCP2 correlated strongly with HAVCR2/TIM-3(ρ=0.847)and lactate metabolism genes,supporting a UCP2-lactate-TAM polarisation axis.TIDE analysis predicted that UCP2-high tumours may be associated with immunotherapy resistance.Multivariate Cox regression confirmed UCP2 as an independent prognostic factor(HR=1.294,95%CI:1.116-1.502,p=6.66×10-4).UCP2 protein expression negatively correlated with Ki67(ρ=−0.446,p=5.23×10-6),and immunofluorescence co-staining(n=6)confirmed co-localisation with CD68-positive TAMs.Conclusion:UCP2 functions as a TAM-intrinsic immune regulator and candidate biomarker for immunosuppressive TME characterisation and immunotherapy response stratification in glioma. 展开更多
关键词 UCP2 glioma tumour-associated macrophages tumour immune microenvironment immune checkpoint predicted immunotherapy resistance single-cell RNA sequencing
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How do mechanical forces impact macrophages in the processes of mechanosensing and mechanotransduction? 认领 引用
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作者 Dan YU Chenlu XU +2 位作者 Jinpeng JIANG Wenyi SHEN Huiyong ZHU 《Journal of Zhejiang University-SCIENCE B》 SCIE CAS CSCD 2026年第2期129-148,共20页
Macrophages are sensitive cells to various external mechanical forces in the environment,such as stretch,shear,and pressure.Mechanical forces can be recognized by mechanical signal receptors on the cell surface,such a... Macrophages are sensitive cells to various external mechanical forces in the environment,such as stretch,shear,and pressure.Mechanical forces can be recognized by mechanical signal receptors on the cell surface,such as cell adhesion molecules and ion channels,and transformed into intracellular biological signals,in turn activating different signaling pathways and thereby regulating the phagocytosis,migration,and polarization of macrophages.The phenomenon in which macrophages transform into different activated phenotypes and perform different functions under varying environmental stimuli is also known as macrophage polarization.In this review,we discuss the roles of mechanically sensitive integrins and ion channels in the mechanical signal sensing of macrophages.We expound on several downstream signaling pathways closely related to integrins and ion channels,such as the nuclear factor-κB(NF-κB),mitogen-activated protein kinase(MAPK),and Yes-associated protein(YAP)ranscriptional co-activator with PDZ-binding motif(TAZ)pathways,which have made good research progress.In addition,we summarize some in vitro experiments on the regulation of macrophage polarization by external mechanical forces,some current cell models for macrophages in vitro,and some commonly used force application devices,with the aim to provide convenience for future in vitro research on macrophages.This paper offers a deep understanding of the mechanical sensitivity and conduction mechanisms of macrophages,which can provide new ideas for the treatment of human diseases. 展开更多
关键词 Macrophage polarization Mechanical force Mechanosensing Mechanotransduction Integrin Transient receptor potential(TRP) Piezo1 Signaling pathway
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TGFβ Blockade by Inhibition of Enolase-1-Mediated Plasmin Targets Tumor-Associated Macrophages in Pancreatic Ductal Adenocarcinoma 认领 引用
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作者 Mao-Lin Chen I-Che Chung +2 位作者 Kevin Chih-Yang Huang K.S.Clifford Chao Ta-Tung Yuan 《Oncology Research》 SCIE 2026年第8期302-325,共24页
Background:Pancreatic ductal adenocarcinoma(PDAC)is characterized by an immunosuppressive and metabolically rewired tumor microenvironment(TME).Althoughα-enolase(ENO1)is frequently overexpressed in PDAC and associate... Background:Pancreatic ductal adenocarcinoma(PDAC)is characterized by an immunosuppressive and metabolically rewired tumor microenvironment(TME).Althoughα-enolase(ENO1)is frequently overexpressed in PDAC and associated with poor prognosis,its functional role in TME remodeling remains unclear.This study investigated the role of ENO1 in plasmin-dependent transforming growth factorβ(TGFβ)activation and metabolic adaptation in PDAC and evaluated the therapeutic potential of HuL001,a first-in-class humanized anti-ENO1 monoclonal antibody.Methods:ENO1 expression and clinical relevance were evaluated in PDAC tissues by immunohistochemistry.Mechanistic studies were performed using PDAC-monocyte co-culture systems,reverse transcription-quantitative PCR(RT-qPCR),enzyme-linked immunosorbent assay(ELISA),flow cytometry,and cell viability assays.The therapeutic effects of HuL001 were further assessed in multiple PDAC xenograft models.Results:Surface ENO1 expression was elevated in advanced PDAC and was associated with poorer overall survival.HuL001 suppressed monocyte-driven PDAC proliferation and reduced factors associated with M2-like macrophages(alternatively activated macrophages),including TGFB1,IL10,and VEGFA.Mechanistically,HuL001 inhibited ENO1-dependent plasmin-mediated activation of latent TGFβand attenuated TGFβ-induced ENO1 expression,plasmin activity,hexokinase 2(HK2)expression,and lactate production.In vivo,HuL001 inhibited PDAC growth and enhanced the antitumor efficacy of gemcitabine in three xenograft models,with greater suppression of tumor growth,intratumoral lactate,and active TGFβthan gemcitabine alone.Conclusion:These findings identify ENO1 as a functional driver of plasmin-dependent TGFβactivation and metabolic adaptation in PDAC and support HuL001 as a promising therapeutic strategy,particularly in combination with gemcitabine. 展开更多
关键词 ENO1 TGFβactivation pancreatic ductal adenocarcinoma monoclonal antibody tumormicroenvironment tumor-associated macrophage
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M2 polarization of macrophages:Manipulation of spinal cord injury repair 认领 引用 被引量：1
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作者 Yiran Lu Hantian Yin +5 位作者 Lingwei Lou Zhonglin Liu Haiming Zhu Chunyi Gu Can Zhang Junjuan Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第9期4195-4210,共16页
Spinal cord injury results in lasting sensory and motor dysfunction with limited regenerative capacity.Macrophages play a crucial role in orchestrating secondary pathogenesis and repair mechanisms through polarization... Spinal cord injury results in lasting sensory and motor dysfunction with limited regenerative capacity.Macrophages play a crucial role in orchestrating secondary pathogenesis and repair mechanisms through polarization dynamics.Following spinal cord injury,these immune cells deploy context-dependent responses via divergent regulatory pathways,mediating phagocytic clearance,inflammatory modulation,and neural tissue remodeling.M1 macrophage polarization exacerbates tissue damage through cytokine storms,reactive oxygen species generation,and subsequent neuronal apoptosis,axonal fragmentation,and glial scarring.Conversely,dominant M2 polarization provides neuroprotection by resolving inflammation and promoting axonal sprouting.Strategic manipulation of macrophage plasticity is a promising frontier in spinal cord injury recovery therapy.This review comprehensively examines the regulatory mechanisms that govern macrophage polarization after spinal cord injury,the functional distinctions between resident microglia and peripheral macrophages,the pathophysiological cascades that occur across injury subtypes,and the emerging interventions that span nanotherapeutics,engineered exosomes,electroactive biomaterials,and photobiomodulation.However,there is still a lack of clinical therapies centered around macrophages due to a lack of human trials targeting macrophage reprogramming and excessive reliance on rodent models without validation in non-human primates.However,given the accelerated development of immunomodulatory biomaterials and the expanding mechanistic insights into polarization pathways,the precision targeting of macrophages warrants prioritized investigation for transformative spinal cord injury therapeutics. 展开更多
关键词 activation biomaterial clinical trial inflammatory macrophage neuron regeneration polarization spinal cord injury therapeutic strategy tissue repair
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Polarizing macrophages derived from human THP-1 cells in vitro:methods and protocols 认领 引用
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作者 Pengfei LI Lin CHEN +2 位作者 Wei YUAN Xingqiang LI Xuesong FENG 《Journal of Zhejiang University-SCIENCE B》 SCIE CAS CSCD 2025年第11期1132-1136,共5页
Macrophages derived from the human THP-1 cell line have been widely used as substitutes for primary macrophages in various macrophage-related studies.However,difficulties still exist in establishing THP-I macrophage m... Macrophages derived from the human THP-1 cell line have been widely used as substitutes for primary macrophages in various macrophage-related studies.However,difficulties still exist in establishing THP-I macrophage models.This research presents techniques for generating different phenotypes of activated macrophages derived from THP-1 cells by introducing specific stimuli and provides some potential markers to confirm each type of activated macrophage.It is hoped to provide novel and useful methods for scientific research and to help researchers explore this field more intuitively and effectively. 展开更多
关键词 polarizing vitro markers generating different phenotypes activated macrophages introducing specific stimuli activation macrophages activated macrophageit
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Inhibiting exosomal miR-191 can induce ferroptosis in macrophages,thereby delaying the progression of colorectal cancer 认领 引用
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作者 Zi-Wei Wang Li Jia +1 位作者 Ling-Ke Qu Guo-Hua Gong 《World Journal of Gastrointestinal Oncology》 SCIE 2026年第5期9-14,共6页
Colorectal cancer(CRC)is a malignant tumor with high incidence and mortality rates.Multiple studies have shown that exosomal miR-191 has an oncogenic role in various cancers.Current evidence suggests that M2 tumor-ass... Colorectal cancer(CRC)is a malignant tumor with high incidence and mortality rates.Multiple studies have shown that exosomal miR-191 has an oncogenic role in various cancers.Current evidence suggests that M2 tumor-associated macrophages(TAMs)are key immunosuppressive cells that induce tumor growth,angiogenesis and epithelial mesenchymal transition.Therefore,M2 TAMs are a potential target for immunotherapy.However,whether CRC-derived exosomal miR-191 can affect CRC progression by altering macrophage polarization has not been reported.Previous studies have predominantly focused on exosomal micro-RNAs that directly regulate tumor cell proliferation,whereas this study reveals the mechanism by which exosomal miR-191 influences macrophage ferroptosis M2 polarization through indirect regulatory pathways.The objective of this study is to explore the association between miR-191,macrophage ferroptosis,and M2-type polarization:(1)Inhibiting miR-191 significantly reduces its expression in colorectal cancer cells and their exosomes,thereby preventing M2 macrophage polarization;(2)Downregulation of miR-191 accelerates ferroptosis to suppress inflammatory responses and M2 polarization of macrophages in colorectal cancer cells;and(3)Exosomes carrying miR-191 from colorectal cancer cells promote disease progression by inducing M2 macrophage polarization. 展开更多
关键词 Colorectal cancer MicroRNA-191 Ferroptosis Reactive oxygen species Macrophage Inflammation
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