Cellular signalling最新文献_第2页

Adaptor protein complex 1 facilitates ciliary localization of serotonin receptor type 6 接头蛋白复合物1促进6型血清素受体的纤毛定位。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-18 DOI: 10.1016/j.cellsig.2025.112008

Yuanyuan Qin , Ko Miyoshi , Zhuoma Yinsheng , Yuuki Fujiwara , Takeshi Yoshimura , Taiichi Katayama

{"title":"Adaptor protein complex 1 facilitates ciliary localization of serotonin receptor type 6","authors":"Yuanyuan Qin , Ko Miyoshi , Zhuoma Yinsheng , Yuuki Fujiwara , Takeshi Yoshimura , Taiichi Katayama","doi":"10.1016/j.cellsig.2025.112008","DOIUrl":"10.1016/j.cellsig.2025.112008","url":null,"abstract":"<div><div>The primary cilium, an immotile protrusion of vertebrate cells, detects chemical and mechanical stimuli in the extracellular milieu and transduces them into the cell body, thereby contributing to cellular development and homeostasis. In the mammalian brain, serotonin receptor type 6 (Htr6) and other specific G protein-coupled receptors (GPCRs) localize preferentially to primary cilia and function in ciliary chemical detection; however, the molecular mechanism by which a subset of GPCRs is transported to primary cilia has not been fully elucidated. In the present study, we demonstrate that a region in the fourth intracellular domain of Htr6 (Htr6 i4) is sufficient for ciliary localization. In yeast, the interaction of this region with the C-terminal region of γ1-Adaptin, a subunit of adaptor protein complex 1 (AP-1), was identified. The interaction between Htr6 and γ1-Adaptin was confirmed by immunoprecipitation analysis using HEK293T cells. The preference for ciliary localization of Htr6 and Htr6 i4 was significantly decreased by ablation of <em>γ1-Adaptin</em> in hTERT RPE-1 cells, which was rescued by exogenous expression of γ1-Adaptin. Furthermore, Htr6 and Htr6 i4 showed reduced localization to primary cilia in <em>γ1-Adaptin</em>-depleted cultured hippocampal neurons compared with control neurons. These results indicate that the ciliary localization of Htr6 is facilitated by AP-1-mediated membrane trafficking.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112008"},"PeriodicalIF":4.4,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to "circPHF16 suppresses prostate cancer metastasis via modulating miR-581/RNF128/Wnt/β-catenin pathway" [Cell Signal. 2023 Feb;102n110557]. “circPHF16通过调节miR-581/RNF128/Wnt/β-catenin通路抑制前列腺癌转移”的更正[Cell Signal. 2023 Feb;102n110557]。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-18 DOI: 10.1016/j.cellsig.2025.111995

Lifeng Ding, Yudong Lin, Xianjiong Chen, Ruyue Wang, Haohua Lu, Huan Wang, Wenqin Luo, Zeyi Lu, Liqun Xia, Xiaobo Zhou, Gonghui Li, Sheng Cheng

引用次数: 0

Epigenetic upregulation of FGF2 promotes glioblastoma progression by enhancing the Warburg effect 表观遗传上调FGF2通过增强Warburg效应促进胶质母细胞瘤的进展。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-18 DOI: 10.1016/j.cellsig.2025.112011

Yefeng Shi , Yang Zhang , Le Xu , Changwei Luo , Shun Xi , Xinyu Xu , Jianquan Liu , Haoyue Xu , Baole Zhang

{"title":"Epigenetic upregulation of FGF2 promotes glioblastoma progression by enhancing the Warburg effect","authors":"Yefeng Shi , Yang Zhang , Le Xu , Changwei Luo , Shun Xi , Xinyu Xu , Jianquan Liu , Haoyue Xu , Baole Zhang","doi":"10.1016/j.cellsig.2025.112011","DOIUrl":"10.1016/j.cellsig.2025.112011","url":null,"abstract":"<div><div>Glioblastoma (GBM), the most common primary intracranial malignancy, remains poorly understood in terms of its underlying etiology. Although fibroblast growth factor 2 (FGF2) is highly expressed in GBM, its epigenetic regulation and functional contributions to disease progression are incompletely defined. Here, through integrated bioinformatics analysis, real-time PCR, and western blot, we demonstrate that FGF2 expression is significantly upregulated in GBM patient-derived tissues and cells. Functional assays revealed that silencing FGF2 markedly suppressed GBM cell proliferation and migration in vitro. Mechanistically, we identified cyclic AMP response element-binding protein 1 (CREB1) as a critical transcription factor regulating <em>FGF2</em> transcription through binding to cAMP response elements (CREs) within the <em>FGF2</em> gene's silencer I and core promoter regions. Intriguingly, these CREs exerted opposing regulatory effects: hypermethylation of the silencer I and hypomethylation of the core promoter favored preferential CREB1 binding to the core promoter in GBM cells. CREB1 recruitment of histone acetyltransferase CBP further promoted histone H3K27 acetylation and enhanced chromatin accessibility at the <em>FGF2</em> core promoter, thereby driving transcriptional activation. Additionally, FGF2 has been shown to significantly enhance glycolysis and lactate production in GBM cells, fueling malignant growth. Collectively, our findings highlight the CREB1/FGF2/lactate axis as a promising therapeutic target for GBM treatment.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112011"},"PeriodicalIF":4.4,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcription factor ZNF207 drives aerobic glycolysis and facilitates malignancy progression in hepatocellular carcinoma 转录因子ZNF207驱动有氧糖酵解并促进肝细胞癌的恶性进展。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-18 DOI: 10.1016/j.cellsig.2025.112009

Chen Chen , Jian-Fei Hu , Bing-Yan Liu , Yi-Min Sun , Bao-Lai Xiao

{"title":"Transcription factor ZNF207 drives aerobic glycolysis and facilitates malignancy progression in hepatocellular carcinoma","authors":"Chen Chen , Jian-Fei Hu , Bing-Yan Liu , Yi-Min Sun , Bao-Lai Xiao","doi":"10.1016/j.cellsig.2025.112009","DOIUrl":"10.1016/j.cellsig.2025.112009","url":null,"abstract":"<div><div>Zinc-finger protein 207 (ZNF207), a prominent member of the zinc finger protein family, exhibits consistent upregulation in various cancer types, including hepatocellular carcinoma (HCC). Unfortunately, the specific oncogenic mechanism of ZNF207 in HCC remains unknown. Our research involved a comprehensive approach, utilizing bioinformatics analysis alongside cell functional experiments, dual-luciferase reporter gene assays, ChIP and qPCR investigations, as well as <em>in vivo</em> studies involving nude mice models for subcutaneous tumor transplantation and tail vein lung metastasis, to delve into the molecular mechanisms underlying its oncogenic properties. The study revealed ZNF207's overexpression in HCC tissues, its correlation with diminished overall survival, and the independent prognostic significance of its expression level in HCC. Furthermore, overexpression of ZNF207 was shown to enhance cell viability, proliferation, and invasive capabilities in HCC cells. Mechanistic analyses pointed towards the modulation of ENO1 and GAPDH transcription by ZNF207, fostering aerobic glycolysis and malignant progression. Subsequent <em>in vivo</em> experiments validated that ZNF207 silencing could impede the growth of subcutaneous tumors and lung metastatic nodules in nude mice, consequently extending their survival. More importantly, Pinosylvin exerts its anti-tumor effects by specifically targeting ZNF207, leading to downregulation of GAPDH and ENO1 expression, inhibition of aerobic glycolysis, and suppression of HCC progression <em>in vitro</em>. In conclusion, these observations highlight ZNF207 as a pivotal oncogene in HCC, with potential for therapeutic targeting in patients with this malignancy.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112009"},"PeriodicalIF":4.4,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144674002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Histone methyltransferase G9a drives ferroptosis to aggravate vascular calcification by inhibiting SLC7A11 transcription 组蛋白甲基转移酶G9a通过抑制SLC7A11的转录，驱动铁下沉加重血管钙化。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-18 DOI: 10.1016/j.cellsig.2025.112010

Qi An , Haoqi Sun , Binhong Yang , Meijuan Cheng , Jingjing Jin , Dongxue Zhang , Lixin Chang , Shenglei Zhang , Yaling Bai , Jinsheng Xu

{"title":"Histone methyltransferase G9a drives ferroptosis to aggravate vascular calcification by inhibiting SLC7A11 transcription","authors":"Qi An , Haoqi Sun , Binhong Yang , Meijuan Cheng , Jingjing Jin , Dongxue Zhang , Lixin Chang , Shenglei Zhang , Yaling Bai , Jinsheng Xu","doi":"10.1016/j.cellsig.2025.112010","DOIUrl":"10.1016/j.cellsig.2025.112010","url":null,"abstract":"<div><div>Vascular calcification (VC) exacerbates the risk of cardiovascular morbidity and mortality in individuals with chronic kidney disease (CKD), and recent advances in pathogenesis have highlighted the significance of ferroptosis. The histone methyltransferase G9a participates in the regulation of different types of cell death including ferroptosis, but its role in VC needs to be further explored. Here, we found that G9a expression was elevated in microarray data obtained from CKD mouse VSMC specimens, and further experiments demonstrated similar results in CKD patients, mouse calcified arteries and rat calcified VSMCs. Functionally, G9a overexpression promoted high calcium and phosphate-induced VSMCs calcification, whereas G9a deficiency had a protective effect. Moreover, our results confirmed that G9a promoted VSMCs calcification through cystine pathway-mediated ferroptosis. Mechanistically, histone H3 lysine 9 dimethylation (H3K9me2) which was catalyzed by G9a, interacted with the promoter of solute carrier family 7 member 11 (SLC7A11) to inhibit its transcription and ferroptosis-related signaling pathways. SLC7A11, a cysteine transporter and ferroptosis suppressor, eliminated the adverse effects of G9a overexpression on ferroptosis and VC in VSMCs. Finally, in vivo overexpression of G9a aggravated VC and ferroptosis in the aorta of CKD mice, accompanied by down-regulation of SLC7A11 expression. In summary, our study reveals that the G9a/H3K9me2/SLC7A11 pathway is a new molecular mechanism for ferroptosis in VC, offering potential guidance for the development of new strategies in the treatment of VC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112010"},"PeriodicalIF":4.4,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of physical exercise on inflammatory profile in chronic renal disease: An overview of the current literature 体育锻炼对慢性肾脏疾病炎症的作用：当前文献综述。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-17 DOI: 10.1016/j.cellsig.2025.112006

Lilian Baseggio , Isabela Berton Wissmann , Renata Cristina Daniel Coelho , Andreia Machado Cardoso

引用次数: 0

Disruption of the actin cytoskeleton with latrunculin A controls ATP-induced nadph oxidase activity and the recruitment of G proteins by neutrophil Gαq-coupled receptors 用拉runculin A破坏肌动蛋白细胞骨架可控制atp诱导的nadph氧化酶活性和中性粒细胞gαq偶联受体募集g蛋白。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-17 DOI: 10.1016/j.cellsig.2025.112005

Neele K. Levin , Claes Dahlgren , Huamei Forsman , Martina Sundqvist

{"title":"Disruption of the actin cytoskeleton with latrunculin A controls ATP-induced nadph oxidase activity and the recruitment of G proteins by neutrophil Gαq-coupled receptors","authors":"Neele K. Levin , Claes Dahlgren , Huamei Forsman , Martina Sundqvist","doi":"10.1016/j.cellsig.2025.112005","DOIUrl":"10.1016/j.cellsig.2025.112005","url":null,"abstract":"<div><div>Signaling by FPR1, the prototype G protein-coupled receptor (GPCR) expressed in neutrophils, is initiated by an activation of a G protein containing a Gα<sub>i</sub> subunit. FPR1 activation results in an increase in the cytosolic concentration of free calcium ions ([Ca<sup>2+</sup>]<sub>i</sub>), and an activation of the NADPH oxidase. Signals generated by the ATP receptor P2Y<sub>2</sub> are transduced by a Gα<sub>q</sub> containing G protein. The neutrophil response induced by ATP includes a transient rise in [Ca<sup>2+</sup>]<sub>i</sub>, but not any activation of the NADPH oxidase. ATP can, however, activate this oxidase through a receptor transactivation mechanism dependent both on P2Y<sub>2</sub>R and on the allosterically modulated free fatty acid receptor FFA2R. The signals whereby FFA2R is activated by the Gα<sub>q</sub>-coupled ATP receptor operate from the cytosolic side of the plasma membrane. Furthermore, in neutrophils with a disrupted actin cytoskeleton, ATP (as well as platelet activating factor; recognized by the Gα<sub>q</sub>-coupled PAFR) potently activates the NADPH oxidase. At high concentrations of the actin cytoskeleton disrupting drug latrunculin A the activation was partly reduced by Gα<sub>q</sub> inhibition as well as by the Gα<sub>i</sub> inhibitor pertussis toxin. The effects on the ATP-induced NADPH oxidase activity, of the Gα<sub>q</sub> inhibitor and pertussis toxin were more and less pronounced, respectively, when the concentration of latrunculin A was reduced. Taken together, we show that the neutrophil actin cytoskeleton is part of the regulatory machinery that determines the activation of the NADPH oxidase and the G protein recruitment profile downstream of activated of two Gα<sub>q</sub>-coupled GPCRs expressed in primary neutrophils.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112005"},"PeriodicalIF":4.4,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Extracellular histone H3 induces macrophage inflammation in acute liver failure via HDAC2 activation and PKM2 subcellular relocalization 细胞外组蛋白H3通过HDAC2激活和PKM2亚细胞再定位诱导急性肝衰竭的巨噬细胞炎症。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-17 DOI: 10.1016/j.cellsig.2025.112003

Danmei Zhang , Jin Guo , Yukun Wang , Xiaoya Zhang , Wen Qu , Luwen Wang , Zuojiong Gong

{"title":"Extracellular histone H3 induces macrophage inflammation in acute liver failure via HDAC2 activation and PKM2 subcellular relocalization","authors":"Danmei Zhang , Jin Guo , Yukun Wang , Xiaoya Zhang , Wen Qu , Luwen Wang , Zuojiong Gong","doi":"10.1016/j.cellsig.2025.112003","DOIUrl":"10.1016/j.cellsig.2025.112003","url":null,"abstract":"<div><div>Acute liver failure (ALF) is a life-threatening clinical syndrome with limited therapeutic options beyond liver transplantation. Extracellular histones, released from dying or activated cells as damage-associated molecular patterns (DAMPs), exert concentration-dependent cytotoxicity and can activate immune cells to trigger inflammatory responses. In the present study, we investigated the impact of extracellular histone H3 on macrophage function during ALF and explored the underlying mechanisms using both in vivo and in vitro models. Extracellular histones stimulation significantly increased inflammation levels in mice. In vitro, H3-treated macrophages adopted a proinflammatory phenotype and exhibited impaired phagocytic capacity. Moreover, H3 stimulation promoted nuclear translocation of PKM2, enhanced glycolytic activity, and upregulated HDAC2 expression in macrophages. Pharmacological inhibition of HDAC2 partially suppressed PKM2 nuclear localization and attenuated macrophage-driven inflammatory responses. Finally, molecular docking and immunofluorescence assays confirmed a direct interaction between HDAC2 and PKM2. Collectively, our findings demonstrate that extracellular histone H3 drives a proinflammatory macrophage phenotype by modulating HDAC2 expression and PKM2 subcellular localization, thereby accelerating the progression of ALF.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112003"},"PeriodicalIF":4.4,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

SNORD46 stabilized by SRSF10 regulating lipid metabolism and cell proliferation of glioma cells via mediating FOXO4 2’-O-methylation SRSF10通过介导FOXO4 2′- o甲基化调节脂质代谢和胶质瘤细胞增殖，从而稳定SNORD46。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-16 DOI: 10.1016/j.cellsig.2025.112002

Tianshu Ying , Xiaobai Liu , Weiwei Dong , Xuelei Ruan , Ping Wang , Libo Liu , Yixue Xue

{"title":"SNORD46 stabilized by SRSF10 regulating lipid metabolism and cell proliferation of glioma cells via mediating FOXO4 2’-O-methylation","authors":"Tianshu Ying , Xiaobai Liu , Weiwei Dong , Xuelei Ruan , Ping Wang , Libo Liu , Yixue Xue","doi":"10.1016/j.cellsig.2025.112002","DOIUrl":"10.1016/j.cellsig.2025.112002","url":null,"abstract":"<div><div>The most common primary malignant tumor of the central nervous system is glioma. One of the key features of malignant tumors is energy reprogramming, which involves changes in lipid metabolism. The objective of our study was to investigate the role of SRSF10, SNORD46, FTSJ3, and FOXO4 in regulating lipid metabolism and proliferation of glioma cells. Our findings revealed a significant increase in the expression of SRSF10, SNORD46, and FTSJ3 in glioma tissues and cells. Knockdown of SRSF10 and SNORD46 led to a reduction in both glioma cell proliferation and lipid metabolism. Furthermore, we discovered that SRSF10 enhanced the stability of SNORD46 by directly binding to it. The study revealed that FTSJ3 functions as a 2’-O-methylation transferase, while SNORD46 downregulated FOXO4 expression by promoting its 2’-O-methylation via FTSJ3. Additionally, FOXO4 suppressed lipid metabolism and cell proliferation in glioma cells by binding to the promoter regions of target genes ACLY and FASN and inhibiting transcription. Furthermore, SRSF10 stabilized SNORD46, which enhanced the SRSF10/SNORD46/FTSJ3/FOXO4 signaling pathway's role as a crucial regulator of glioma cell proliferation and lipid metabolism, presenting potential therapeutic targets for glioma treatment.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112002"},"PeriodicalIF":4.4,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Recent advances in the crosstalk between bone and vascular system: from mechanism to therapy 骨与血管系统串扰的研究进展：从机制到治疗。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-15 DOI: 10.1016/j.cellsig.2025.112001

Zhuoxuan Su , Jiali Liu , Zhensen Zheng , Luoxi Zhen , Xin Hu , Duosheng Luo

{"title":"Recent advances in the crosstalk between bone and vascular system: from mechanism to therapy","authors":"Zhuoxuan Su , Jiali Liu , Zhensen Zheng , Luoxi Zhen , Xin Hu , Duosheng Luo","doi":"10.1016/j.cellsig.2025.112001","DOIUrl":"10.1016/j.cellsig.2025.112001","url":null,"abstract":"<div><div>Osteoporosis and cardiovascular disease are prevalent health concerns, particularly among the elderly. Recent studies have increasingly demonstrated that osteoporosis is consistently associated with vascular calcification, drawing attention to the interactions between bones and blood vessels, and giving rise to the concept of the bone-vascular axis. The bone vascular axis involves several factors, including osteokines such as FABP3, PDGF-BB, MYGDF, and Aging Bone-Derived Extracellular Vesicles (AB-EVs), which influence vascular calcification. Simultaneously, calcified blood vessels secrete sclerostin, Dickkopf1 (Dkk-1), Activin-A, and frizzled-related protein (SFRP), further affecting bone metabolism. The bone-vascular axis is characterized by reciprocal regulation and influence between the skeletal and vascular systems, and is crucial for maintaining bone metabolic homeostasis and preventing cardiovascular disease. However, the causal relationship between these two systems, as well as the specific regulatory mechanisms and targets, remains unclear. Therefore, this review aims to explore the mechanisms underlying the crosstalk between bone and blood vessels from both the skeletal and vascular perspectives, as well as their common pathways, and to provide an overview of current therapeutic agents, with the goal of enhancing understanding of the bone-vascular association and offering new insights and approaches for clinical treatment.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112001"},"PeriodicalIF":4.4,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0