Current Medical Science最新文献

{"title":"Multi-Omics Analysis Reveals Inflammatory Activation and Maternal-Fetal Interface Remodeling in Spontaneous Abortion.","authors":"Yan-Juan Huang, Zou-Qin-Xuan Shen, Dan-Ping Hu, Ying-Yuan Huang, Guang-Yu Chen, Ying Lin, Bang-Mei Hu, Xiao-Xiao Yuan, Gao-Pi Deng, Xing Li","doi":"10.1007/s11596-026-00195-8","DOIUrl":"https://doi.org/10.1007/s11596-026-00195-8","url":null,"abstract":"<p><strong>Background: </strong>Spontaneous abortion (SA) is a common adverse outcome of early pregnancy, yet its underlying pathophysiological mechanisms remain incompletely understood. Accumulating evidence suggests that dysregulated inflammatory responses at the maternal-fetal interface play a critical role in pregnancy loss. However, the potential associations between alterations in gut microbiota, metabolic disturbances, and localized decidual inflammation in patients with SA have not been systematically characterized.</p><p><strong>Methods: </strong>Women with SA (n = 30) and those with normal early pregnancy (NP, n = 28) were enrolled in this study. Proinflammatory cytokines were quantified in decidual tissue homogenates, and histopathological and molecular analyses were performed to evaluate inflammatory activation at the maternal-fetal interface. The gut microbiota composition was profiled using shotgun metagenomic sequencing, while metabolic alterations in the feces were assessed by untargeted metabolomics. Integrated multi-omics analyses were conducted to explore associations among gut microbial dysbiosis, metabolic perturbations, decidual inflammatory signaling, and molecular alterations.</p><p><strong>Results: </strong>Compared with those from the NP group, the decidual tissues from the SA group exhibited significantly elevated levels of IL-1β and TNF-α (1.49-fold and 1.51-fold, both P < 0.0001), accompanied by pronounced histopathological abnormalities. Enhanced activation of the NF-κB signaling pathway was observed at the maternal-fetal interface in SA patients. Metagenomic analyses revealed distinct differences in the gut microbiota composition and community structure between the two groups, with differentially abundant bacterial taxa identified (LDA score > 2.0). Consistent with these findings, fecal metabolomic profiling clearly revealed differences between SA and NP patients, with differentially abundant metabolites (VIP > 1.0, adjusted P < 0.05) predominantly enriched in lipid metabolism, amino acid metabolism, and immune-related pathways. In addition, the expression of leucine-rich repeat-containing G protein-coupled receptor 6 was significantly upregulated (P < 0.0001) in the decidual tissue of SA patients.</p><p><strong>Conclusions: </strong>These findings indicate that SA is associated with localized inflammatory activation at the maternal-fetal interface, dysregulation of decidual molecular activity, gut microbiota dysbiosis, and metabolic perturbations. Integrated multi-omics analyses suggest potential interactions among these factors that may be linked to decidual dysfunction during early pregnancy, providing new insights into the complex pathophysiology of SA.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk Factors for Idiopathic Premature Ovarian Insufficiency.","authors":"Fan Li, Yan-Jing Huang, Yu-Li Geng, Ru-Nan Hu, Ming-Min Zhang","doi":"10.1007/s11596-026-00205-9","DOIUrl":"https://doi.org/10.1007/s11596-026-00205-9","url":null,"abstract":"<p><p>Premature ovarian insufficiency (POI) is a harmful disease that leads to decreased fertility and osteoporosis and an increased risk of cardiovascular disease. POI seriously affects women's physical and mental health. Currently, the incidence of POI is rising; however, the etiology of most cases remains unclear, and these cases are referred to as idiopathic POI. Understanding the risk factors for idiopathic POI is beneficial for preventing and recognizing POI early on, as well as for improving treatment outcomes. This paper describes the etiology and pathogenesis of idiopathic POI from five perspectives: genetic and familial factors; environmental factors (including endocrine-disrupting chemicals, persistent organic pollutants, and heavy metals); gut microbial disorders; lifestyle factors (including smoking, diet, physical activity, and pathological sleep); and psychological and social factors. Furthermore, this review discusses the interactions among these risk factors and provides clinical prevention recommendations. This study aims to improve clinical diagnosis and treatment of idiopathic POI and women's health.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated DNA Repair Capacity and NER Gene Expression for Improving Risk Prediction in Head and Neck Squamous Cell Carcinoma.","authors":"Ling Zhang, Yi-Qian Liang, Xiao-Rong Niu, Fang Sui, Yan-Xia Bai, Shao-Qiang Zhang, Hai-Yan Cai, Xiao-Tong Zhang, Peng Han","doi":"10.1007/s11596-026-00202-y","DOIUrl":"https://doi.org/10.1007/s11596-026-00202-y","url":null,"abstract":"<p><strong>Objective: </strong>DNA repair plays a critical role in the development of smoking-related cancers. We hypothesized that DNA repair capacity (DRC) and nucleotide excision repair (NER) mRNA expression are associated with increased head and neck squamous cell carcinoma (HNSCC) risk in the Chinese population.</p><p><strong>Methods: </strong>We conducted a case-control study including 349 patients with HNSCC and 316 cancer-free controls. DRC and NER mRNA expression levels were measured in lymphoblastoid cells exposed to benzo[a]pyrene diol epoxide (BPDE). Correlations between DRC and NER mRNA expression were analyzed, and their associations with HNSCC risk were evaluated.</p><p><strong>Results: </strong>The mean DRC was significantly lower in patients with HNSCC (9.72% ± 2.25%) than in healthy controls (10.81% ± 2.63%, P < 0.001). Compared with individuals with higher DRCs, those with lower DRCs had a significantly greater risk of HNSCC (odds ratio [OR] = 2.23, 95% confidence interval [CI] = 1.60-3.10, P < 0.001; P_trend < 0.001). Correlation analyses demonstrated significant associations between DRC and the expression of XPA and XPB. Moreover, predictive models combining DRC with XPA and/or XPB mRNA expression significantly improved risk prediction, as evidenced by increased area under the curve (AUC) values (P < 0.05).</p><p><strong>Conclusions: </strong>Suboptimal DRC and reduced expression of key NER genes, particularly XPA and XPB, are associated with increased HNSCC risk. Integrating these two NER biomarkers may provide a novel and improved model for HNSCC risk assessment.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Nomogram for Predicting Meningioma Grade Based on Radiomics Features and Clinical Characteristics.","authors":"Peng-Fei Yan, Bao-Ping Zheng, Ye Yuan, Zhen Zhao, Hao-Jun Shi, Dong-Xiao Yao","doi":"10.1007/s11596-026-00199-4","DOIUrl":"https://doi.org/10.1007/s11596-026-00199-4","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to develop a predictive model utilizing radiomics features and clinical characteristics to accurately differentiate low-grade (WHO grade I) from high-grade (WHO grade II/III) meningiomas preoperatively, thereby improving treatment planning and prognosis.</p><p><strong>Methods: </strong>A retrospective analysis of 288 meningioma cases (191 low-grade and 97 high-grade) confirmed by histopathology was conducted. Radiomics features were extracted from contrast-enhanced T1-weighted MRI (CE-T1WI) using the pyradiomics package, followed by feature selection via LASSO regression. Predictive models (logistic regression, decision tree, support vector machine [SVM], adaptive boosting) were evaluated. Clinical variables (peritumoral edema index and monocyte count) were integrated to try to improve the predictive performance. Model efficacy was assessed using receiver operating characteristic (ROC) curves, calibration plots, and decision curve analysis.</p><p><strong>Results: </strong>Four key radiomics features were identified as significant discriminators of tumor grade. The logistic regression model demonstrated superior predictive performance over decision trees, SVMs, and adaptive boosting methods. The inclusion of the peritumoral edema index and monocyte count increased the AUC to 0.801 (95% CI 0.753-0.869) in the training set. However, in the validation set, the radiomics model achieved the best performance, with an AUC of 0.770 (95% CI 0.670-0.869).</p><p><strong>Conclusions: </strong>The radiomics-based model effectively predicts high-grade meningioma and demonstrates superior performance compared to the clinical and combined models. This study advances the precision of meningioma grading, offering significant implications for treatment planning and patient management.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the Gut Microbiota-Bile Acid-FXR Axis: The Therapeutic Mechanism of Yudantong Decoction in Cholestatic Liver Disease.","authors":"Xiao-Ming Wu, Lin-Yi Hou, Chang Liu, Yan Hu, Qiang He","doi":"10.1007/s11596-026-00191-y","DOIUrl":"https://doi.org/10.1007/s11596-026-00191-y","url":null,"abstract":"<p><strong>Objective: </strong>To elucidate the therapeutic mechanism of Yudantong decoction (YDTD) in cholestatic liver disease (CLD), focusing on the gut microbiota-bile acid-intestinal farnesoid X receptor (FXR) axis.</p><p><strong>Methods: </strong>A CLD mouse model induced by α-naphthylisothiocyanate was treated with YDTD. Hepatic injury, gut microbiota composition (16S rRNA sequencing), bile acid profiles (high-performance liquid chromatography-tandem mass spectrometry, HPLC-MS/MS), intestinal FXR/NLRP3 signaling, and barrier function were assessed. Fecal microbiota transplantation, bile salt hydrolase (BSH) inhibition, and FXR antagonism were employed for mechanistic validation.</p><p><strong>Results: </strong>CLD mice exhibited hepatocellular steatosis, lobular necrosis, and elevated serum markers. These pathological changes were associated with gut dysbiosis, impaired bile acid metabolism via bile salt hydrolase (BSH) suppression, FXR signaling inhibition, and NLRP3 inflammasome activation. YDTD restored BSH activity and bile acid homeostasis, upregulated FXR expression, suppressed NLRP3 inflammasome activation, and improved intestinal barrier integrity. Fecal microbiota transplantation experiments confirmed that YDTD-modified microbiota mediated these therapeutic benefits, whereas pharmacological inhibition of BSH or FXR attenuated YDTD's therapeutic effects.</p><p><strong>Conclusion: </strong>YDTD alleviates CLD, at least in part, by targeting the gut microbiota-bile acid-FXR signaling pathway, highlighting the gut microbiota as a promising therapeutic target for CLD.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From Bench to Bedside: Neurofilament Light Chain as a Biomarker in Ischemic Stroke.","authors":"Khiany Mathias, Anita Dal Bó Tiscoski, Francieli Vuolo, Maria Amélia Cechinel, Naíla Maciel Andrade, Fabricia Petronilho","doi":"10.1007/s11596-026-00200-0","DOIUrl":"https://doi.org/10.1007/s11596-026-00200-0","url":null,"abstract":"<p><p>Neurofilaments (NFs) are protein structures that form part of the neuronal cytoskeleton, providing structural support and facilitating axonal transport. Neurofilament light chain (NFL) has emerged as a promising biomarker for various neurological conditions, as it is released into the bloodstream following neuronal damage. The ability of NFL to differentiate between types of injury and enhance the accuracy of clinical prediction models makes it an asset in both clinical practice and research. Studies suggest that NFL can be employed to diagnose and monitor disease progression and aid in the prognosis of various neurological conditions, including ischemic stroke (IS). In IS, NFL serves as a predictor of severity, functional recovery, and the risk of complications. This review therefore synthesizes current preclinical and clinical studies on the use of NFL as a biomarker for prognosis, monitoring, and treatment in IS.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E2F Accelerates the Proliferation of B-Cell Non-Hodgkin Lymphomas by Upregulating Cell-Cycle Genes.","authors":"Si-Ying Liu, De-Dong Zhang, Ya-Qin Wang, Wen Yu, Li Wang, Jia-Si Zhang, Ai-Guo Liu","doi":"10.1007/s11596-026-00181-0","DOIUrl":"https://doi.org/10.1007/s11596-026-00181-0","url":null,"abstract":"<p><strong>Objective: </strong>The high toxicity of current therapies and frequent relapse in mature B-cell non-Hodgkin lymphomas (B-NHLs) reveal a substantial unmet clinical need for more effective targeted treatment strategies. To address this gap, Gene Set Enrichment Analysis (GSEA) of B-NHL datasets was conducted, uncovering marked enrichment of E2F transcription factors and their target genes. Despite the central role of E2F signaling in cell cycle control and oncogenesis, its contribution to pediatric B-NHLs has not been systematically characterized. Accordingly, we performed a comprehensive analysis of E2F signaling and its downstream targets to identify potential therapeutic and prognostic biomarkers in pediatric B-NHLs.</p><p><strong>Methods: </strong>The datasets used for this analysis were obtained from the Gene Expression Omnibus (GEO) database, and mRNA and protein expression levels were further validated via data from The Cancer Genome Atlas (TCGA), Gene Expression Profiling Interactive Analysis (GEPIA), and the Human Protein Atlas (HPA). Key bioinformatics findings were validated via quantitative PCR (qPCR) and cell proliferation assays. Survival analysis was conducted to evaluate the associations between gene expression levels and the prognosis of B-NHL patients. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and GSEA were employed to predict gene functions and associated pathways.</p><p><strong>Results: </strong>Childhood B-NHLs were markedly enriched for E2F gene set. The identified overlapping differentially expressed genes (DEGs) were linked to cell cycle regulation, DNA replication, and proliferative activity. E2F1 and hub genes such as POLD1, LIG1, MCM3, MCM6, and PCNA were markedly overexpressed in B-cell lymphoma. These genes demonstrated strong discriminatory potential as disease-associated signaling molecules. Moreover, the expression of POLD1 was closely associated with the proliferative capacity of B-NHLs.</p><p><strong>Conclusion: </strong>E2Fs and their downstream target genes are significantly overexpressed in pediatric B-NHLs, driving tumor cell proliferation. These molecules may serve as biomarkers for therapeutic stratification, prognosis, and disease monitoring in pediatric B-NHLs.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Non-traditional Lipid Indices and Sarcopenia: Evidence from a Prospective Chinese Cohort Study.","authors":"Rui-Rong Pan, Rui-Xue Tang, Zi-Fan Qian, Jun-Yan Gong","doi":"10.1007/s11596-026-00193-w","DOIUrl":"https://doi.org/10.1007/s11596-026-00193-w","url":null,"abstract":"<p><strong>Objective: </strong>Recent study links sarcopenia with lipid metabolism disorders. This study aimed to examine the associations between non-traditional lipid indices-specifically the lipoprotein combined index (LCI) and the non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (non-HDL-C to HDL-C ratio, NHHR)-and incident sarcopenia in a Chinese population.</p><p><strong>Methods: </strong>Participants aged ≥ 45 years were enrolled from the 2011-2015 waves of the China Health and Retirement Longitudinal Study (CHARLS). Multivariate logistic regression was applied in cross-sectional analyses (n = 3,161) to assess the associations between log-transformed LCI, NHHR and sarcopenia. Longitudinal analyses (n = 2,898) were performed using multivariate Cox proportional hazards models, restricted cubic splines, subgroup analyses, and receiver operating characteristic (ROC) curves. Sensitivity analyses were conducted to test the robustness of the results.</p><p><strong>Results: </strong>Higher quartiles of lnLCI and lnNHHR were inversely associated with sarcopenia in both cross-sectional (lnLCI Q4: OR 0.58, P = 0.015; lnNHHR Q3: OR 0.56, P = 0.005) and longitudinal analyses (lnLCI Q4: HR 0.57, P = 0.001; lnNHHR Q4: HR 0.46, P = 0.002), with linear trends observed in spline models. Alcohol intake modified the association between lnNHHR and sarcopenia (P = 0.017), whereas the association of lnLCI with sarcopenia remained consistent in alcohol intake subgroup. ROC analyses showed similar predictive ability (lnLCI AUC 0.599; lnNHHR AUC 0.603). Sensitivity analyses excluding participants with hypercholesterolemia further validated the findings.</p><p><strong>Conclusions: </strong>Among Chinese adults aged ≥ 45 years, LCI and NHHR were inversely associated with sarcopenia, with NHHR demonstrating slightly superior diagnostic potential.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-Scale Genetic and Transcriptomic Analyses Identify Druggable Targets for Epilepsy.","authors":"Gao-Yang Zhong, Cong Liu, Hui-Ling Wang, Man Liang, Zi-Long Liu","doi":"10.1007/s11596-026-00194-9","DOIUrl":"https://doi.org/10.1007/s11596-026-00194-9","url":null,"abstract":"<p><strong>Background: </strong>Epilepsy is a common neurological disorder with high genetic heterogeneity and affects approximately 70 million people worldwide. Although several studies have combined Genome-Wide Association Studies (GWAS) with bulk expression quantitative trait loci (eQTLs) to explore epilepsy risk genes, the cellular context of genetic regulation remains insufficiently defined.</p><p><strong>Methods: </strong>We integrated epilepsy GWAS data with brain bulk and single-cell eQTLs using summary-data-based Mendelian randomization (SMR) and Bayesian colocalization to identify causal genes. The identified genes were validated in an independent RNA-seq cohort of patients with refractory epilepsy. We then characterized cell-type specificity and intercellular signaling using single-cell RNA sequencing (scRNA-seq) and CellChat. Druggability and drug-repurposing analyses were performed using DSigDB to identify targeted therapeutic compounds for epilepsy.</p><p><strong>Results: </strong>Seven epilepsy causal genes (FGFR3, PM20D1, ZNF564, HAGH, CAPN15, CCDC117 and DARS1-AS1) were identified, with FGFR3 and HAGH identified as druggable targets. FGFR3 was predominantly expressed in astrocytes and involved in an astrocyte-centered FGF2-FGFR signaling loop, whereas HAGH was enriched in neurons. DSigDB analysis highlighted the FGFR inhibitor, Ro-4396686, as the top candidate compound.</p><p><strong>Conclusions: </strong>Multi-scale integration of eQTL, GWAS and transcriptomic datasets reveals the genetic variants of epilepsy, with FGFR3-driven FGF signaling representing a principal molecular axis. This study reveals the cellular context of this disorder and highlights FGFR3 and HAGH as promising therapeutic targets.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic Regulation of Macrophage Polarization for Diabetic Kidney Disease by Targeted Metabolic Reprogramming.","authors":"Si-Ying Fei, Rui-Tong Liu, Wen-Xiao Yang, Bing-Shu Wu, Xiao-Bin Mei, Mao-Jin Xu","doi":"10.1007/s11596-026-00192-x","DOIUrl":"https://doi.org/10.1007/s11596-026-00192-x","url":null,"abstract":"<p><p>Diabetic kidney disease (DKD) is one of the most common microvascular complications of diabetes. It can be identified by thickening of the glomerular basement membrane, reduced glomerular filtration rate, and persistent proteinuria. Macrophages play a key role in the pathogenesis of DKD, and their phenotype (M1 and M2) is finely regulated by metabolic reprogramming. M1 macrophages exacerbate inflammatory damage and fibrosis in renal tissue by secreting pro-inflammatory mediators and reactive oxygen species (ROS). M2 macrophages (further subdivided into M2a, M2b, M2c and M2d subtypes) primarily exert anti-inflammatory and tissue-repairing effects. Of these, the M2a and M2c subtypes are particularly crucial for anti-inflammatory repair. This study aimed to systematically review the mechanisms by which glucose, lipid, amino acid, and mitochondrial function-related metabolism influence macrophage polarization. It further explored therapeutic strategies to mitigate renal inflammation and fibrosis by regulating macrophage polarization through targeted metabolic pathways, including inhibiting glycolysis, promoting fatty acid oxidation, modulating amino acid metabolism, and enhancing mitochondrial biogenesis and oxidative phosphorylation (OXPHOS). Several natural compounds and synthetic drugs exhibit the potential to induce M2 polarization and suppress M1 polarization through metabolic reprogramming, thereby offering new directions for optimizing therapeutic strategies for DKD.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}