Cytokine最新文献

{"title":"Unraveling the immune activation mechanisms of DAMPs in coronary artery disease through transcriptomic and single-cell analyses","authors":"Yinghao Li,&nbsp;Henghe Shi,&nbsp;Yifei Zou,&nbsp;Yinuo Guan,&nbsp;Ning Liu,&nbsp;Bin Liu","doi":"10.1016/j.cyto.2025.156952","DOIUrl":"10.1016/j.cyto.2025.156952","url":null,"abstract":"<div><div>This study employs transcriptomics and single-cell analysis to delve into the mechanisms by which damage-associated molecular patterns (DAMPs) trigger immune activation in coronary artery disease (CAD). We obtained RNA-seq data from the GSE202625 and GSE242046 datasets, as well as single-cell RNA-seq data from the GSE159677 dataset, all sourced from the GEO database. Through differential expression analysis, we identified 821 differentially expressed genes (DEGs), comprising 389 upregulated and 432 downregulated genes, which are likely closely associated with the pathological processes of CAD. Notably, the genes P2RY14 and IFIH1 exhibited significant expression differences in CAD, suggesting their potential involvement in immune responses and inflammatory processes. Our findings indicate a significant infiltration and activation of immune cells in CAD patients, particularly T cells and macrophages. The activation of these cells is likely linked to the release of DAMPs and the activation of pattern recognition receptors (PRRs), thereby triggering local and systemic inflammatory responses. Single-cell analysis further revealed distinct clustering patterns of immune cells, especially T cells and B cells, in CAD patients compared to healthy controls. Dendritic cells and macrophages play particularly critical roles in the development of CAD. Dendritic cells bridge innate and adaptive immune responses by presenting antigens to T lymphocytes, potentially either promoting or inhibiting the progression of atherosclerosis. Macrophages exhibit polarization during the atherosclerosis process, with M1-type macrophages tending to promote inflammatory responses, while M2-type macrophages may exert anti-inflammatory effects.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156952"},"PeriodicalIF":3.7,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Augmented hippocampal up-regulation of immune modulators following a peripheral immune challenge in a hemizygous mouse model of the 15q13.3 microdeletion","authors":"Katherine A. Rees ,&nbsp;Kristin M. McCamy ,&nbsp;Conner I. Danao,&nbsp;Ursula H. Winzer-Serhan","doi":"10.1016/j.cyto.2025.156951","DOIUrl":"10.1016/j.cyto.2025.156951","url":null,"abstract":"<div><div>The strongest known genetic risk factor for generalized epilepsy is the human hemizygous 15q13.3 microdeletion (MD). This 1.5 Mb MD encompasses six genes, including CHRNA7 encoding the alpha7 subunit that forms the homo-pentameric nicotinic acetylcholine receptor, a known regulator of the immune system. In the CNS, hyper activation of neuroimmune responses contributes to increased seizure susceptibility. In a mouse model with a hemizygous deletion of the orthologous region (Df(h15q13)/+) (Het), we previously demonstrated increased hippocampal expression of inflammatory cytokines compared to wildtype (WT) mice following a mild peripheral immune challenge. To further characterize neuroimmune responses, hippocampal mRNA expression of the chemokines CXCL2 and CXCL10, and the Gap junction protein connexin 43 (GJA1), all of which are implicated in neuronal hyperexcitability, were determined along with additional immune related targets. Three hours after a lipopolysaccharide (LPS, 0.1 mg/kg) or polyinosinic:polycytidylic acid (Poly(I:C), 5 mg/kg) injection (i.p.), hippocampi were collected, mRNA extracted, and cDNA prepared for qPCR. The results demonstrate extensive upregulation of CXCL2 and CXCL10 expression by LPS and Poly(I:C) (up to 200-fold CXCL2, up to 600-fold CXCL10) (<em>p</em> &lt; 0.0001) with genotype x treatment interactions for CXCL2 by LPS (<em>p</em> &lt; 0.007). Responses to treatment were far smaller in magnitude for all other targets. LPS and Poly(I:C) induced statistically similar increases for Toll-like receptor (TLR)2, TLR4, HMGB1, and C3, but Poly(I:C) had stronger effects on GJA1, TLR3, C1qA and MARCO expression. Remarkably, TLR3 was the only target with significant downregulation of expression after Poly(I:C) (<em>p</em> &lt; 0.0001). In addition, genotype x treatment interactions were detected for TLR3, TLR4, HMGB1, and C1qA (<em>p</em> &lt; 0.02). Thus, a peripheral immune challenge caused extensive increases for CXCL2 and CXCL10, and the genotype-treatment interactions that was seen for several targets, underscored the augmented neuroinflammatory response in mice carrying the MD. Of note is the dramatic upregulation of CXCL10 by low dose Poly(I:C). CXCL10 causes hyperexcitability via neuronal CXCR3 activation. Thus, even an asymptomatic viral infection may increase seizure susceptibility. In summary, a peripheral immune challenge causes strong upregulation of hippocampal inflammatory mediators implicated in neuronal excitability which is particularly detrimental for individuals with high seizure susceptibility, such as carriers of the 15q13.3 MD.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156951"},"PeriodicalIF":3.7,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-4 exerts beneficial anti-tumor effect dependent on a short-range manner","authors":"J.D. Zhang ,&nbsp;X.Y. Xue ,&nbsp;Y.F. Zhang ,&nbsp;S.Q. Lin ,&nbsp;Z.J. Sun ,&nbsp;L.X. Yan ,&nbsp;Y.G. Zhang ,&nbsp;W. Wang","doi":"10.1016/j.cyto.2025.156950","DOIUrl":"10.1016/j.cyto.2025.156950","url":null,"abstract":"","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156950"},"PeriodicalIF":3.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-inflammatory effects of apigenin on LPS-induced mastitis in lactating SD rats through inhibiting TLR4/NF-κB signaling pathway","authors":"Yihan Hu ,&nbsp;Yingying Xie ,&nbsp;Yiming Sun ,&nbsp;Linghuan Luo ,&nbsp;Haibin Wang ,&nbsp;Ruili Zhang ,&nbsp;Ming Ge","doi":"10.1016/j.cyto.2025.156944","DOIUrl":"10.1016/j.cyto.2025.156944","url":null,"abstract":"<div><div>Mastitis is an important disease of the mammary gland in all kinds of lactating mammals, endangering the development of animal husbandry and human health. Apigenin is one chemical constituent of Taraxacum and Philippine Violet Herb which are effective Chinese herbs for the treatment of mastitis. It is reported that apigenin possesses anti-inflammatory activity and other pharmacological effects. However, the attenuation of apigenin on mastitis has not yet been reported. The present study investigated the protection of apigenin against lipopolysaccharide (LPS)-induced mastitis in SD rats both in vivo and in vitro. The results suggested that apigenin relieved the lesions of mammary tissues induced by LPS, decreased mRNA and protein levels of pro-inflammatory cytokines:tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Simultaneously, apigenin reduced the increasing content of myeloperoxidase (MPO) and Toll-like receptor 4 (TLR4), and phosphorylation of nuclear factor kappa B (NF-κB) induced by LPS. The results showed that apigenin was able to attenuate the LPS-induced mastitis in rats by inhibiting the TLR4/NF-κB signaling pathway in vivo and in vitro, which provides scientific references for further research.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156944"},"PeriodicalIF":3.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The mechanism of action of GLUT1 in promoting NETs-mediated impairment of macrophage phenotypic switching based on macrophage-fibroblast interplay","authors":"Wenqiang Li ,&nbsp;Shijie Li ,&nbsp;Weijing Sun,&nbsp;Dezhi Han","doi":"10.1016/j.cyto.2025.156946","DOIUrl":"10.1016/j.cyto.2025.156946","url":null,"abstract":"<div><div>This study explored the mechanism by which glucose transporter type 1 (GLUT1) promotes neutrophil extracellular trap (NET)-mediated macrophage phenotype conversion in a high-glucose environment, based on the interaction between fibroblasts and macrophages. We demonstrated that GLUT1 plays an important role in immune cell–fibroblast crosstalk. High glucose induces GLUT1 to upregulate high mobility group box 1 (HMGB1) levels, thereby promoting NET release and macrophage M1 polarization. Addition of a NET inhibitor promoted macrophage M2 polarization and alleviated the impaired macrophage phenotype conversion. Additionally, overexpression of <em>Glut1</em> enhanced the expression of inflammatory factors tumor necrosis factor alpha (TNF-α) and interleukin beta (IL-1β), leading to inflammatory damage to fibroblasts, which was reversed significantly by inhibiting NETs . The results indicated that GLUT1 mediates the crosstalk between NETs, macrophage phenotype conversion impairment, and inflammatory damage in fibroblasts. This study emphasizes the importance of GLUT1 in the interaction between immune cells and fibroblasts, and its regulatory role in the impairment of NET-mediated macrophage phenotype conversion. These findings suggest that the regulatory mechanisms between HMGB1 and NETs in a high-glucose environment might provide potential therapeutic targets to treat diabetic wounds.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156946"},"PeriodicalIF":3.7,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143860276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From genes to clinic: Genomic and cross-sectional cohort analysis of oxidative stressors and lipid metabolism in European ancestry","authors":"Bo He ,&nbsp;Yingjie Li ,&nbsp;Ning Zhou","doi":"10.1016/j.cyto.2025.156941","DOIUrl":"10.1016/j.cyto.2025.156941","url":null,"abstract":"<div><h3>Background</h3><div>The link between oxidative stress and lipid metabolism is widely studied, but their causal relationship in the general population remains unclear.</div></div><div><h3>Methods</h3><div>We utilized weighted regression and propensity score matching (PSM) models to investigate the relationship between endogenous oxidative stress markers (serum bilirubin and uric acid) and lipid metabolism in 11,087 participants of European ancestry from the National Health and Nutrition Examination Survey (NHANES) during the period from 2005 to 2018. Additionally, we performed a bidirectional two-sample Mendelian randomization (MR) analysis using Genome-Wide Association Study (GWAS) summary statistics from individuals of European ancestry (<em>n</em> = 997 to 575,531) to explore the genetic causal relationship between oxidative stress markers and lipid metabolism profiles (<em>n</em> = 20,430).</div></div><div><h3>Results</h3><div>Weighted regression showed that serum uric acid significantly increased high cholesterol (OR = 1.11, 95 % CI = 1.06–1.15, <em>P</em> &lt; 0.001) and high triglycerides (OR = 1.25, 95 % CI = 1.20–1.30, <em>P</em> &lt; 0.001). PSM analysis confirmed that serum uric acid increased the incidence of high triglycerides (OR = 1.57, 95 % CI = 1.35–1.82, P &lt; 0.001). Additionally, a strong bidirectional genetic relationship was found between oxidative stress markers and lipid metabolism. For example, serum uric acid increased serum triglycerides (β = 0.1904, Se = 0.05, <em>P</em> &lt; 0.001) and decreased total cholesterol in very large HDL (β = −0.1298, Se = 0.039, <em>P</em> &lt; 0.001). Conversely, total cholesterol reduced direct bilirubin levels (β = −0.1707, Se = 0.018, P &lt; 0.001). No significant horizontal pleiotropy was detected by MR-Egger intercept.</div></div><div><h3>Conclusion</h3><div>Our findings demonstrate a robust genetic and population-based association between oxidative stress markers and lipid metabolism, suggesting potential therapeutic targets for lipid disorders based on endogenous oxidative stressors.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156941"},"PeriodicalIF":3.7,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic insights into neuroblastoma: the role of immune cell features","authors":"Yunfei Ma ,&nbsp;Qiang He ,&nbsp;Yan Su ,&nbsp;Wen Zhao ,&nbsp;Cheng Huang ,&nbsp;Jing Qin ,&nbsp;Shengjie You ,&nbsp;Yan Hu ,&nbsp;Xin Ni","doi":"10.1016/j.cyto.2025.156942","DOIUrl":"10.1016/j.cyto.2025.156942","url":null,"abstract":"<div><h3>Objective</h3><div>To elucidate the causal relationship between immune cells and neuroblastoma, we conducted a two-sample Mendelian randomization (MR) analysis.</div></div><div><h3>Materials and methods</h3><div>The exposure and outcome data for the genome-wide association study (GWAS) used in this research were sourced from an open-access database. The study utilized two-sample MR analysis to evaluate the causal relationship between 731 immune cell features and neuroblastoma. The main approach to explore this relationship is to apply the inverse variance weighting (IVW) method. In addition, sensitivity analyses including leave-one-out analysis, Cochran's Q test, Mendelian randomization Egger method (MR-Egger) intercept test and Mendelian randomization pleiotropy residual sum and outlier test (MR-PRESSO) were performed to verify the reliability of the MR results.</div></div><div><h3>Results</h3><div>The study identifies five immune cell traits as causally contributing to neuroblastoma risk, including CD3⁻ lymphocyte (% of leukocytes) (IVW: OR[95 % CI] 0.65[0.42–0.99], <em>P</em> = 0.0469), CD86 on granulocyte (IVW: OR[95 % CI] 0.61[0.41–0.92], <em>P</em> = 0.0167), FSC-A on granulocyte(IVW: OR[95 % CI] 0.73[0.57–0.93], <em>P</em> = 0.0117), HLA DR+ CD8+ T cell Absolute Count(IVW: OR[95 % CI]: 1.38[1.01–1.88], <em>P</em> = 0.0408), IgD− CD38+ B cell Absolute Count(IVW: OR[95 % CI] 0.42[0.27–0.66], <em>P</em> = 0.0002). The results of sensitivity analyses were consistent with the main findings.</div></div><div><h3>Conclusion</h3><div>We demonstrated a close causal relationship between specific types of immune cells and neuroblastoma by genetic methods, offering valuable guidance for future clinical studies.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156942"},"PeriodicalIF":3.7,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of GFPT2 enhances cisplatin chemotherapy sensitivity in STK11/KRAS mutant non-small cell lung cancer by regulating the hexosamine biosynthesis pathway, resisting tumor growth","authors":"Cheng Zhang ,&nbsp;Xuelei Yin ,&nbsp;Jun Jiang ,&nbsp;Peng Wang ,&nbsp;Yirong Wang","doi":"10.1016/j.cyto.2025.156943","DOIUrl":"10.1016/j.cyto.2025.156943","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the role of GFPT2 in the sensitivity of STK11/KRAS lung cancer cells to cisplatin chemotherapy, and its underlying mechanism.</div></div><div><h3>Materials &amp; methods</h3><div>A549 and H460 cells were used to analyze the effect of GFPT2 on cisplatin chemotherapy sensitivity, as both carry KRAS mutations and H460 has LKB1 inactivation mutations, meeting the requirements of a KRAS/LKB1 co mutant tumor model. The levels of UDP-GlcNAc, OGT, OGA, and O-GlcNAc in the HBP pathway were also determined. To verify the potential role of HBP, we added OGT inhibitors. In vivo, we constructed a nude mouse model bearing A549 tumor to further validate the results of in vitro cell experiments.</div></div><div><h3>Results</h3><div>GFPT2 silencing can significantly inhibit cell proliferation, invasion, and migration, promote cell apoptosis, and enhance the effect of cisplatin (<em>p</em> &lt; 0.05). After OSMI-1 processing, GFPT2 enhances O-GlcNAc modification levels via the OGT-mediated HBP, thereby decreasing the sensitivity of STK11/KRAS mutant cells to cisplatin chemotherapy. In addition, GFPT2 silencing enhances the chemotherapy sensitivity of cisplatin and inhibits tumor growth, while overexpression of GFPT2 weakens this effect (<em>p</em> &lt; 0.05). The above results provide new targets and combination therapy options for the clinical treatment of KRAS/LKB1 mutant lung cancer.</div></div><div><h3>Conclusion</h3><div>Our study found that inhibiting GFPT2 can enhance the chemotherapy sensitivity of cisplatin to STK11/KRAS/LKB1 mutant NSCLCs cells through the OGT mediated HBP pathway, filling a key gap in the chemotherapy resistance mechanism of KRAS/LKB1 mutant lung cancer.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156943"},"PeriodicalIF":3.7,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC00426 promotes the progression of atherosclerosis by regulating miR-873-5p/SRRM2 axis","authors":"Bo Zhou ,&nbsp;Lu Gan ,&nbsp;Pimo Zhou ,&nbsp;Tai Yang ,&nbsp;Fang Tang ,&nbsp;Peng Jin ,&nbsp;Ping Jin ,&nbsp;Jiulin Chen","doi":"10.1016/j.cyto.2025.156938","DOIUrl":"10.1016/j.cyto.2025.156938","url":null,"abstract":"<div><h3>Background</h3><div>Atherosclerosis (AS) is a disease that occurs in the great arteries and is the main cause of cardiovascular disease and death.</div></div><div><h3>Objective</h3><div>To investigate the clinical significance of LINC00426 in AS and to investigate that LINC00426 regulates PDGF-BB-induced proliferation, migration, invasion and inflammatory response of vascular smooth muscle cells (VSMCs) by modulating miR-873-5p/SRRM2 axis.</div></div><div><h3>Methods</h3><div>The expression of LINC00426 was detected using RT-qPCR. The diagnostic role of LINC00426 in AS was analyzed with ROC curves. CCK-8 assay was used to measure cell proliferation, and transwell assay was used to measure cell migration and invasion ability. The targeted binding relationship between LINC00426 and miR-873-5p, miR-873-5p and SRRM2 was detected using dual-luciferase reporter gene assay. The concentration of proinflammatory factors was detected by using ELISA kit.</div></div><div><h3>Result</h3><div>The expression of LINC00426 was increased in patients with AS, and LINC00426 had a diagnostic role in AS. In addition, LINC00426 regulated PDGF-BB-induced proliferation, migration, invasion, and inflammation of VSMCs by regulating miR-873-5p/SRRM2 axis.</div></div><div><h3>Conclusion</h3><div>LINC00426 may function as a biomarker for the diagnosis and treatment of AS.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156938"},"PeriodicalIF":3.7,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143829460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotinamide metabolism affects the prognosis of hepatocellular carcinoma by influencing the tumor microenvironment","authors":"Min Zhou ,&nbsp;Wenhui Zhao ,&nbsp;Xiaobo Zhang ,&nbsp;Ye Cheng ,&nbsp;Mengxiang Wang ,&nbsp;Yan Chen ,&nbsp;Lingrui Zhao","doi":"10.1016/j.cyto.2025.156939","DOIUrl":"10.1016/j.cyto.2025.156939","url":null,"abstract":"<div><div>In this study, we utilized the public database along with single-cell genomics techniques to systematically analyze the expression patterns and clinical significance of key genes in the nicotinamide metabolism pathway in liver cancer samples. The findings indicate that differential nicotinamide metabolism-related key genes are expressed in liver cancer samples. The liver cancer samples were put into separate subgroups using consistency clustering analysis based on differential gene expression levels observed. Additionally, immune infiltration and drug sensitivity analysis also revealed differences between the two subgroups. Survival analysis suggested that the key genes were associated with prognosis. Finally, a prognostic model was established using the key genes, offering a fresh viewpoint on the molecular mechanism investigating liver cancer. This study demonstrated the significant correlation between key genes in the nicotinamide metabolism pathway and the occurrence and progression of liver cancer and indicated that these key genes could serve as prognostic markers and tailored treatment targets for liver cancer.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156939"},"PeriodicalIF":3.7,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}