Cellular signalling最新文献

{"title":"Therapeutic potential of ghrelin and synthetic GHS for heart failure from the perspective of its protective effect on cardiomyocytes","authors":"Qiang Sun ,&nbsp;Chen Chen","doi":"10.1016/j.cellsig.2025.111956","DOIUrl":"10.1016/j.cellsig.2025.111956","url":null,"abstract":"<div><div>Endogenous ghrelin and its synthetic mimetics are peptide growth hormone (GH) secretagogues (GHSs) that exert a variety of cardioprotective effects. There are experimental evidence suggesting the beneficial effects of GHSs on ischemia/ reperfusion (I/R) injury, myocardial infarction (MI), heart failure (HF), isoproterenol-induced injury, and doxorubicin-induced cardiotoxicity. The effects of GHS were mediated by improving contractility and cardiac output, vasodilation, boosting cardiac antioxidant potential, reducing infarct size, and inhibition of cardiac apoptosis and fibrosis. The existing literatures have confirmed the improvement of cardiac function, attenuation of inflammation, rebalancing the autonomic nervous system (ANS), suppression of cardiac remodeling, improving arrhythmia and HF by GHS in experimental animal models and clinical patients. However, the molecular mechanisms of GHS on HF have not been fully elucidated. Here, we summarize available recent data on improving HF by GHS through molecular signaling pathways, to propose a novel strategy for the prevention and treatment of HF.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111956"},"PeriodicalIF":4.4,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144338715","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}

{"title":"LARS1 lactylation inhibits autophagy by activating mTORC1 to promote podocytes injury in diabetic kidney disease","authors":"Zhibin Fan ,&nbsp;Yue Zhang ,&nbsp;Liming Yuan ,&nbsp;Yuan Gao ,&nbsp;Xiaoxi Tian ,&nbsp;Jin Tian ,&nbsp;Jie Wan ,&nbsp;Bingyu Li ,&nbsp;Xiaoqi Wang ,&nbsp;Shuo Wang ,&nbsp;Lianshan Zhang ,&nbsp;Lei Wang ,&nbsp;Pengxiang Zhou ,&nbsp;Wei Liu","doi":"10.1016/j.cellsig.2025.111955","DOIUrl":"10.1016/j.cellsig.2025.111955","url":null,"abstract":"<div><div>Diabetic kidney disease (DKD) progression is predominantly attributed to podocyte injury. However, the underlying mechanisms remain inadequately understood. DKD patients exhibit elevated lactate concentrations due to impaired glucose metabolism. Lactate serves as a substrate for a post-translational modification known as lactylation, which is integral to numerous cellular processes. The study aimed to explore the potential role of lactylation in DKD podocyte injury and to elucidate its underlying mechanisms. The results showed that lactate concentrations were elevated in the plasma of DKD patients, as well as in the serum and renal tissue of diabetic mice. High glucose (HG) resulted in increased lactate accumulation in podocytes, exacerbated podocyte injury and promoted protein lactylation. Protein modification omics demonstrated that LARS1 lactylation was enhanced, specifically at the K970 site, which further aggravated podocyte injury by inhibiting autophagy and promoting apoptosis. In vivo transfection with LARS1 siRNA significantly improved renal function and mitigated podocyte injury. Our study identified a novel mechanism linking LARS1 lactylation activity to compromised podocyte autophagy, heightened podocyte injury, and the onset of proteinuria within DKD.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111955"},"PeriodicalIF":4.4,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144365133","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}

{"title":"K33 only mutant ubiquitin augments cisplatin chemoresistance in A549 and NCI-H446 cells via Akt1 K33 ubiquitination","authors":"Yi Zhen Yin ,&nbsp;Hong Ying Yang ,&nbsp;Yi Yun Liang ,&nbsp;Xiao Yan Liao ,&nbsp;Jun Jun Jia ,&nbsp;Xiao Jie Chen ,&nbsp;Jing Yi Wu ,&nbsp;Rui Ling Chen ,&nbsp;Feng Guang Gao","doi":"10.1016/j.cellsig.2025.111959","DOIUrl":"10.1016/j.cellsig.2025.111959","url":null,"abstract":"<div><h3>Background</h3><div>To probe the function of Akt1 K33 ubiquitination in cisplatin-induced apoptosis in lung cancer.</div></div><div><h3>Methods</h3><div>Akt1 K33 ubiquitination modified by MG132/PYR-41, K33 only mutant ubiquitin (K33O), and Akt1 silence was investigated by co-immunoprecipitation in A549 and NCI-H446 cells. Akt phosphorylation was interrogated by western blot. The role of Akt1 K33 ubiquitination in cisplatin-induced apoptosis was assessed by cell viability using crystal violet staining, the changes of mitochondrial membrane potential with Rhodamine 123 (Rho123) and Calcein AM staining, and cell apoptosis with flow cytometric assay via annexin V-PI staining, respectively.</div></div><div><h3>Results</h3><div>Cisplatin induced apoptosis in A549 and NCI-H446 cells; K33O reversed the cisplatin resistance with elevated K33 ubiquitination; The intervention with Wortmannin induced a significant attenuation in the Akt phosphorylation; Inhibiting Akt1 K33 ubiquitination abolished cisplatin effects on cell viability, manifesting as heightened apoptosis and alterations in mitochondrial membrane potential.</div></div><div><h3>Conclusions</h3><div>Akt1 K33 ubiquitination emerges as a promising therapeutic target for lung cancer chemotherapy.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111959"},"PeriodicalIF":4.4,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144366428","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}

{"title":"Unraveling m6A RNA methylation: From epitranscriptomics to therapeutic frontiers in renal cell carcinoma","authors":"Tingfei Xie ,&nbsp;Jiahui Chen ,&nbsp;Xiaolu Sui,&nbsp;Yunpeng Xu,&nbsp;Aisha Zhang,&nbsp;Yanzi Zhang,&nbsp;Jihong Chen","doi":"10.1016/j.cellsig.2025.111952","DOIUrl":"10.1016/j.cellsig.2025.111952","url":null,"abstract":"<div><div>N6-methyladenosine (m6A) RNA methylation has emerged as a crucial regulatory mechanism in cancer biology, influencing processes such as RNA splicing, stability, translation, and degradation. Renal cell carcinoma (RCC), often referred to as a silent cancer, is one of the most common malignancies of the urinary tract and is associated with poor prognosis and inadequate treatment options. m6A modifications play a pivotal role in RCC tumorigenesis, metastasis, progression, immune response modulation, and therapy resistance. This review provides a comprehensive overview of the current understanding of m6A in RCC, discussing key m6A regulators and their roles as potential biomarkers and therapeutic targets. Furthermore, we explore advanced technologies like single-cell omics and machine learning in elucidating the role of m6A in RCC, facilitating the search for effective therapeutic targets. Future directions focus on translating these findings into clinical applications, with a view toward personalized medicine and combination therapies.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111952"},"PeriodicalIF":4.4,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144367990","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}

{"title":"Nuclear adenomatous polyposis coli elevates STAT1 and reduces CXCL1,2, and 3 expression and inhibits neutrophil recruitment","authors":"Alexander Q. Sandoval,&nbsp;Anika James,&nbsp;Kristi L. Neufeld","doi":"10.1016/j.cellsig.2025.111957","DOIUrl":"10.1016/j.cellsig.2025.111957","url":null,"abstract":"<div><div>Adenomatous polyposis coli (<em>APC</em>) mutations and chronic inflammation can each promote colon cancer. Though both mice and humans with germline <em>APC</em> mutations show reduced tumorigenesis if treated with anti-inflammatory agents, direct links between APC and inflammation remain incomplete. In the current study, we examine a novel role for APC in intestinal inflammation via inhibition of neutrophil-recruiting chemokines CXCL1, 2, and 3. Patients with colorectal adenocarcinoma, the majority of whom would be expected to harbor <em>APC</em> mutations, showed upregulated CXCL1, 2, and 3 expression at early stages of disease. APC induction in cultured human colon cells reduced levels of CXCL1 and CXCL2 proteins and <em>CXCL1</em>, <em>CXCL2</em>, and <em>CXCL3</em> RNAs and increased expression of signal transducer and activator of transcription 1 (<em>STAT1</em>), a potential negative regulator of <em>CXCL1</em> transcription. By mining published Chromatin-immunoprecipitation sequencing (ChIP-Seq) data, we found regions of the <em>STAT1</em> promoter and upstream CpG island as APC-bound. Methylation-specific PCR and bisulfite sequencing each revealed decreased methylation of the <em>STAT1</em> CpG island upon APC induction. Intestinal tissue explants from mice compromised for nuclear Apc (Apc^mNLS/mNLS) secreted more CXCL1 and CXCL2 than wild-type explants. Conditioned media from APC-expressing cells recruited fewer neutrophils in a trans-well migration assay. In vivo, colon and ileal tissues from Apc^mNLS/mNLS mice displayed more neutrophils than Apc^+/+ mice. Experimental evidence from in vitro and in vivo systems validates that nuclear APC can inhibit inflammation by suppressing neutrophil-recruiting chemokines CXCL1, 2, and 3, potentially via epigenetic regulation of <em>STAT1</em>. These findings offer a new target for managing inflammation in inflammatory bowel disease and reveal a new mechanism by which APC loss enables cancer progression.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111957"},"PeriodicalIF":4.4,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144367989","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}

{"title":"Distribution of macrophages in the cochlea following radiation-induced sensorineural hearing loss","authors":"Yiming Gao ,&nbsp;Guisheng Chen ,&nbsp;Junbo Wang ,&nbsp;Ziyi Cai ,&nbsp;Jiaqi Pang ,&nbsp;Yiqing Zheng","doi":"10.1016/j.cellsig.2025.111958","DOIUrl":"10.1016/j.cellsig.2025.111958","url":null,"abstract":"<div><div>Radiation-induced sensorineural hearing loss (RISNHL) is a common and irreversible complication of radiotherapy for head and neck tumors, with currently no effective treatment. While traditional research has primarily focused on the direct effects of radiation on cochlear hair cells (HCs), this alone does not explain the early onset of hearing loss observed before HC degeneration. Emerging evidence from our preliminary study suggests that the pathogenesis of RISNHL may be driven by significant microenvironmental alterations within the cochlea, particularly involving dysfunction of the stria vascularis (SV) and changes in macrophage activity. However, the precise mechanisms underlying radiation-induced cochlear damage remain unclear. In this study, we investigated the dynamic changes in cochlear macrophages from 2 to 20 weeks (w) following ionizing radiation (IR). Our results revealed a time-dependent increase in IBA1-positive macrophages in both the cochlear lateral wall and spiral ganglion, peaking between 12 and 20 w. Further analysis showed significant macrophage accumulation and activation in the SV region following localized irradiation. Proteomic profiling identified upregulated expression of ADAM17 in the SV at both 1 and 8 w post-IR, indicating a potential role for immune processes in radiation-induced cochlear injury. These findings highlight the critical role of macrophages in post-radiation cochlear damage. Our study systematically characterizes the spatiotemporal progression of radiation-induced cochlear damage and offers insights into novel intervention strategies that could be applied before irreversible HC loss occurs.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111958"},"PeriodicalIF":4.4,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144367988","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}

{"title":"FAAP100:A biomarker based on pan-cancer analysis, promotes the progression of lung adenocarcinoma","authors":"Di Wu ,&nbsp;Min Gao ,&nbsp;Baochen Zhou ,&nbsp;Chunyang Zhu ,&nbsp;Yingxu Luo ,&nbsp;Fan Xia ,&nbsp;Xinran Wang ,&nbsp;Haiteng Liu ,&nbsp;Xin Zheng","doi":"10.1016/j.cellsig.2025.111950","DOIUrl":"10.1016/j.cellsig.2025.111950","url":null,"abstract":"<div><div>FAAP100 plays an essential role in DNA damage repair, with dysregulation associated with elevated cancer susceptibility. Nevertheless, comprehensive pan-cancer analyses examining FAAP100 prognostic significance, immune correlations, and epigenetic regulation remains unexplored. This study systematically characterized FAAP100 across 33 cancer types utilizing multi-omics data from TCGA, UALCAN, cBioPortal, TIMER2.0, and CPTAC. Analytical assessments included expression profiles, prognostic significance, and diagnostic utility, alongside associations with DNA methylation, immune cell infiltration, immune checkpoint gene expression, tumor mutational load (TMB), microsatellite instability (MSI), and drug resistance. Findings revealed significant FAAP100 upregulation across multiple cancer types, exhibiting inverse correlations to patient survival. Genomic characterization identified associations between FAAP100 overexpression and both copy number amplification and promoter hypomethylation. Immune profiling demonstrated robust correlations with immune cell infiltration levels and checkpoint molecule activity. Functional assays utilizing PC9 and H1299 cells indicated that FAAP100 enhances cellular proliferation and migration while inhibiting apoptosis processes. In vivo studies confirmed tumor growth suppression upon FAAP100 knockdown. Collectively, this multi-omics investigation identifies FAAP100 as a pan-cancer oncogene driver, highlighting its potential as both a prognostic biomarker and therapeutic target. The integrated analysis of expression patterns, epigenetic modifications, immune characteristics, and genomic alterations elucidates the mechanistic involvement of FAAP100 in tumor progression, providing a foundation for clinical application in precision oncology approaches..</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111950"},"PeriodicalIF":4.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144322206","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}

{"title":"IL-10 alleviates ulcerative colitis by regulating mitochondrial function through reducing ISG15 expression","authors":"Zhi He ,&nbsp;Ya-dong Feng ,&nbsp;Yue-xin Zhang ,&nbsp;Xun Gao ,&nbsp;Jing-jing Liu ,&nbsp;Shuang Liu ,&nbsp;Guo-qiu Wu","doi":"10.1016/j.cellsig.2025.111932","DOIUrl":"10.1016/j.cellsig.2025.111932","url":null,"abstract":"<div><h3>Background</h3><div>Interleukin-10 (IL-10), an anti-inflammatory cytokine, has shown therapeutic effect on autoimmune diseases, yet its effects on UC remain unclear. This study aims to investigate whether the administration of IL-10 can suppress disease flares in ulcerative colitis (UC).</div></div><div><h3>Methods</h3><div>A UC model was established in mice using dextran sulfate sodium (DSS) to evaluate the therapeutic effect of IL-10. LPS-stimulated Caco-2 cells were utilized to explore the underlying molecular mechanisms, focusing on apoptosis, inflammation, and oxidative stress.</div></div><div><h3>Results</h3><div>IL-10 administration significantly alleviated clinical symptoms in DSS-induced colitis, including promoting body weight recovery, increasing colon length, and reducing disease activity index scores. IL-10 repaired the intestinal mucosal barrier by inhibiting apoptosis of intestinal epithelial cells, downregulating pro-inflammatory cytokines (IL-6, Interferon-γ, and IL-1β), and modulating oxidative stress markers, such as malondialdehyde (MDA) and superoxide dismutase (SOD). In LPS-stimulated Caco-2 cells, IL-10 protected against apoptosis, oxidative stress, and inflammation. Bioinformatics analysis of control and IL-10 knockout mice showed a significant upregulation of Interferon-Stimulated Gene 15 (ISG15) after IL-10 knockout. In contrast, ISG15 expression was downregulated in the LPS + IL-10 group but upregulated in LPS-stimulated Caco-2 cells. These results suggest that ISG15 is a target gene of IL-10 and plays a role in autophagy regulation. Furthermore, IL-10 enhanced autophagy by increasing the protein expression of ATG7, and the LC3-II/LC3-I ratio, thereby reducing apoptosis and oxidative stress in Caco-2 cells. Autophagy inhibition with 3-Methyladenine or overexpression of ISG15 diminished IL-10's protective effects.</div></div><div><h3>Conclusion</h3><div>This study demonstrates that IL-10 administration inhibits the progression of UC by activating autophagy and modulating ISG15 expression. In the future, targeted delivery of IL-10 to the intestinal lamina propria may enhance therapeutic efficacy while minimizing systemic side effects.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111932"},"PeriodicalIF":4.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336368","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}

{"title":"Insights on the role of the chemokine CCL8 in pathology","authors":"Bernardo Chavez ,&nbsp;Hippokratis Kiaris","doi":"10.1016/j.cellsig.2025.111951","DOIUrl":"10.1016/j.cellsig.2025.111951","url":null,"abstract":"<div><div>Chemokine (C-C motif) ligand 8 (CCL8), also known as monocyte chemotactic protein-2 (MCP-2) is involved in immune cell recruitment, inflammation, and disease progression. While essential for host defense, dysregulated CCL8 expression and signaling contribute to the progression of infectious diseases, inflammatory disorders, and various cancers. CCL8 is also transcriptionally regulated under hypoxic conditions, linking it to the remodeling of the tumor microenvironment, placental dysfunction, and ischemic injury. In infections such as HIV, tuberculosis, and viral pneumonias, CCL8 regulates immune cell trafficking, enhancing both pathogen clearance and excessive immune activation. Inflammatory conditions such as graft-versus-host disease (GVHD), idiopathic pulmonary fibrosis (IPF), and preeclampsia are also associated with elevated CCL8 expression, promoting immune dysregulation and tissue damage. In allergic diseases such as asthma and atopic dermatitis, CCL8 contributes to Th2-driven inflammation by recruiting eosinophils and CCR8⁺ T cells to affected tissues. In cancer, CCL8 promotes tumor progression, metastasis, immune evasion, and therapeutic resistance through the recruitment of immunosuppressive cells such as M2 macrophages and regulatory T cells. Given its widespread role in immune modulation, CCL8 represents both a potential diagnostic biomarker and a therapeutic target. Recent advances in antibody-based therapies and ligand-directed strategies, including cytotoxic CCL8 analogs, highlight new opportunities for translational application. Further research is needed to clarify its specific mechanisms and explore targeted interventions that modulate CCL8 signaling for clinical applications.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111951"},"PeriodicalIF":4.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336369","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}

{"title":"Glycolytic reprogramming in macrophage polarization: New horizons in the treatment of tumor diseases","authors":"Dong Wang ,&nbsp;Haoran Guan","doi":"10.1016/j.cellsig.2025.111940","DOIUrl":"10.1016/j.cellsig.2025.111940","url":null,"abstract":"<div><div>Macrophages serve as sentinels on the front line of tissue defense, acting as essential components of the body's arsenal against invading pathogens. Their metabolic modes and functions are closely linked to the progression and regression of diseases. Typically, macrophages preferentially utilize the glycolytic pathway for energy production, with glycolysis being particularly dominant in hypoxic environments. Notably, tumor-associated macrophages (TAMs) also rely on glycolysis for energy production even in the presence of sufficient oxygen, a phenomenon known as the classic \"Warburg effect.\" TAMs play a critical role in the development and progression of malignant tumors, including angiogenesis, and are considered a key component of the tumor microenvironment (TME). They promote tumor growth, invasion, metastasis, and tumor neoangiogenesis. The infiltration level and polarization status of TAMs within the tumor stroma are closely associated with patient prognosis and represent potential targets for tumor immunotherapy. Furthermore, tumor growth is heavily dependent on tumor neoangiogenesis. In this paper, we systematically reviewed the literature on macrophages and tumor therapy to elucidate and summarize the relationship between the glycometabolic mechanisms of macrophage polarization and tumors. This review aims to provide theoretical guidance for tumor treatment and the development of antitumor drugs.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111940"},"PeriodicalIF":4.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144338817","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}