Current Medical Science最新文献

{"title":"Nanomaterial Platforms for Endometriosis: A Systematic Review.","authors":"Hong-Yu Chen, Na Li, Xiao-Dan Zhu, Xiang-Cheng Pan, En-Yuan Tian, Fang-Fang Lang, Wei Tian","doi":"10.1007/s11596-026-00239-z","DOIUrl":"https://doi.org/10.1007/s11596-026-00239-z","url":null,"abstract":"<p><p>Endometriosis (EM) is a chronic, estrogen-dependent inflammatory disease affecting approximately 10% of women of reproductive age worldwide, causing debilitating pelvic pain, infertility, and substantially impaired quality of life. Conventional hormonal therapies and surgery are limited by systemic side effects, high recurrence rates, and failure to maintain adequate drug concentrations at ectopic lesion sites. Nanotechnology-based drug delivery has emerged as a promising strategy for directing therapeutic agents to ectopic lesion sites, potentially reducing the systemic toxicity that limits current pharmacological options. We systematically review three nanomaterial platforms-hydrogels, extracellular vesicles (EVs), and inorganic nanoparticles-with attention to their physicochemical properties, therapeutic rationale, and preclinical findings, as well as the specific strengths and unresolved limitations of each platform. We further compare how each platform addresses the core pathological processes of EM, namely, persistent inflammation, progressive fibrosis, and pathological angiogenesis. We hope that this review will assist researchers in comparing nanocarrier strategies and identifying more realistic pathways for clinical application in EM.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618622","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":"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":"616-636"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13315473/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL3-m⁶A-LOXL2 Axis Post-Transcriptionally Fine-Tunes Macrophage Migration and Invasion.","authors":"Zheng Li, Xiao-Han Sa, Yu-Wen Han, Pu Wang, Xue-Yan Song, Min-Xuan Sun","doi":"10.1007/s11596-026-00204-w","DOIUrl":"10.1007/s11596-026-00204-w","url":null,"abstract":"<p><strong>Objective: </strong>While the RNA modification N⁶-methyladenosine (m⁶A) is known to influence immune cell function, its specific role in regulating macrophage migration and invasion remains poorly defined. This study aimed to elucidate the function and mechanism of the core m⁶A methyltransferase METTL3 in the migratory and invasive capacities of macrophages.</p><p><strong>Methods: </strong>A macrophage-specific METTL3-knockdown model was established. The functional effects of METTL3 deficiency were systematically evaluated using migration, invasion, phagocytosis, and polarization assays. Subsequent transcriptome sequencing (RNA-seq) and methylated RNA immunoprecipitation-quantitative PCR (MeRIP-qPCR) were employed to identify the key differentially expressed gene, lysyl oxidase-like 2 (LOXL2). This mechanistic link was ultimately confirmed through functional rescue experiments and reconstitution assays.</p><p><strong>Results: </strong>METTL3 deficiency significantly increased the migratory and invasive capacities of macrophages but attenuated their phagocytic activity, promoting a shift toward an M2-like polarization state. Mechanistically, METTL3 knockdown reduced m⁶A modification at a specific site of LOXL2 mRNA, thereby decreasing its RNA stability and leading to decreased expression. Importantly, this phenotype was validated through functional inhibition assays. Reconstitution of LOXL2 in METTL3-deficient macrophages substantially reversed the enhanced migratory and invasive phenotypes.</p><p><strong>Conclusion: </strong>This study reveals a novel METTL3-m⁶A-LOXL2 signaling axis that posttranscriptionally fine-tunes macrophage migration and invasion by regulating gene expression. These findings provide a mechanistic explanation for the functional dynamics of macrophage migration and invasion and underscore that m⁶A modification is a key regulator of innate immune cell behavior.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"725-738"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027859","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":"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":"771-783"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","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":"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":"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":"791-801"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","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":"Decoding the Histomorphological and Multi-Omic Characteristics of Melanotic Schwannoma.","authors":"Yi Jiang, Rui Zhao, Hang Xian, Lin Shi, Jin-Kang Zhang, Song-Lin Li, Ye Peng, Jun-Jie Du, Rui Cong, Han Wang","doi":"10.1007/s11596-026-00197-6","DOIUrl":"10.1007/s11596-026-00197-6","url":null,"abstract":"<p><strong>Objective: </strong>Melanotic schwannoma (MS) is a rare peripheral nerve sheath tumor accompanied by melanin deposition and severe refractory pain. However, its molecular pathogenesis remains unclear. This study aimed to explore the histomorphological, transcriptomic, and proteomic characteristics of MS, and to identify key molecules related to melanin production, pain generation, and targeted therapy.</p><p><strong>Methods: </strong>Histomorphological characteristics of MS were observed by Luxol Fast Blue (LFB) staining and hematoxylin and eosin (HE) staining in tumor tissues from 3 MS patients. Combined transcriptomic and proteomic analyses were performed to screen differentially expressed genes and proteins. The expression levels of tyrosinase-related protein 1 (TYRP1), transient receptor potential ankyrin 1 (TRPA1), and Bruton's tyrosine kinase (BTK) were validated by quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, and immunofluorescence staining.</p><p><strong>Results: </strong>Histomorphological examination revealed typical melanin deposition and prominent compression of adjacent nerve fibers in MS. Transcriptomic and proteomic analyses showed activation of the melanin synthesis pathway and transient receptor potential (TRP) channel-related neuroinflammatory pathway. The expression of TYRP1 and TRPA1 was significantly upregulated, suggesting that these related pathways are associated with melanin production and neuropathic pain in MS. In addition, the expression of BTK, a known molecular target of targeted drugs, was significantly increased, suggesting that BTK inhibitors have potential therapeutic effects on MS.</p><p><strong>Conclusion: </strong>This study delineates the histomorphological features, transcriptomic and proteomic profiles of MS. TYRP1, TRPA1, and BTK are identified as key molecules involved in melanogenesis, pain generation, and targeted therapy, respectively. These findings provide novel insights into the pathogenesis and potential therapeutic strategies for MS.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"690-703"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13314831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","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":"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":"802-814"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13315467/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Burden and Long-Term Trends of Viral Hepatitis in China: A National and Provincial Analysis.","authors":"Jing-Yi Peng, Xin-Yu Xiang, Jie Zhang, Yuan Yuan, Yang Ding, Yu-Chen Xia, You-de Xiao, Xing-Xing He","doi":"10.1007/s11596-026-00211-x","DOIUrl":"10.1007/s11596-026-00211-x","url":null,"abstract":"<p><strong>Objective: </strong>Viral hepatitis remains a major global health threat, causing approximately 1.3 million deaths in 2022. Despite substantial advances in vaccination and clinical treatment, it continues to impose a heavy disease burden across China. Existing studies have largely focused on single hepatitis subtypes and national epidemiological trends, with limited evidence on provincial heterogeneity. To fill this research gap, this study aimed to conduct a refined, region-specific epidemiological assessment of viral hepatitis in China.</p><p><strong>Methods: </strong>Data were extracted from the Global Burden of Disease Study 2021 (GBD 2021) and the China Public Health Science Data Center to systematically analyze the epidemiological characteristics and spatiotemporal trends of viral hepatitis in China over the past three decades.</p><p><strong>Results: </strong>The overall burden of viral hepatitis in China decreased substantially over the study period, with obvious regional heterogeneity. Acute hepatitis A, B and E, as well as chronic hepatitis B and C, all presented prominent downward trends. The fastest declines in incidence were observed in acute hepatitis B (estimated annual percentage change [EAPC] = -3.03) and chronic hepatitis B (EAPC = -4.74). Notably, males suffered a higher disease burden for nearly all outcomes, except for HCV-related hepatocellular carcinoma, which predominantly affected females. Furthermore, provincial-level analysis indicated marked regional disparities: Xizang maintained a high incidence rate, while Beijing exhibited low incidence accompanied by strikingly high hepatitis-related mortality, suggesting a notable decoupling between infection prevalence and mortality.</p><p><strong>Conclusions: </strong>China has achieved remarkable reductions in the overall burden of viral hepatitis, attributable to comprehensive public health interventions such as universal vaccination, standardized screening and improved sanitation conditions. Nevertheless, residual burdens in vulnerable populations and striking regional inequalities warrant targeted prevention and control strategies to reduce disease disparities nationwide.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"828-842"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148223557","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":"Does Voclosporin Redefine Lupus Nephritis Treatment? A Tri-Focal View of Efficacy, Safety, and Costs.","authors":"Ting-Ting Zhuo, Meng-Hao Li, Xin-Hui Zhang, Yun-Fei Tian, Bo-Kun Chen, Ze-Kun Kang, Xiu-Ju Liu","doi":"10.1007/s11596-026-00217-5","DOIUrl":"10.1007/s11596-026-00217-5","url":null,"abstract":"<p><p>Lupus nephritis (LN) is a frequent and severe manifestation of systemic lupus erythematosus (SLE) that substantially affects renal outcomes and long-term survival. Notably, this disease remains a leading cause of SLE-related mortality. Glucocorticoids, hydroxychloroquine, immunosuppressive agents, and calcineurin inhibitors (CNIs) represent the standard therapy. As a next-generation CNI, the use of voclosporin represents a therapeutic advance for LN. This can be attributed to its optimized pharmacologic properties and dual mechanism of action, which involves potent inhibition of T-cell activation and direct stabilization of podocytes. In pivotal phase III trials, the addition of voclosporin to a background of mycophenolate mofetil and low-dose glucocorticoids significantly increased complete renal remission rates and produced a rapid, durable reduction in proteinuria. These findings support a \"low steroid\" treatment approach. Compared with conventional CNIs, voclosporin has more consistent pharmacokinetics, favorable metabolic safety, and lacks clinically meaningful drug-drug interactions with mycophenolate mofetil. Voclosporin is also cost effective, as suggested by economic evaluations conducted from multiple national health-system perspectives. The available evidence collectively indicates that voclosporin, through its efficacy, safety, and economic value, enables a more precise, efficient, and comparatively cost-effective treatment paradigm for LN.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"677-689"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204420","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":"Microbiota-Derived Metabolites in Developmental Programming: Bridging Early-Life Gut Microbiota to Childhood Metabolic Disorders.","authors":"Li-Wen Liao, Xiao-Tong Gou, Wei Xia","doi":"10.1007/s11596-026-00213-9","DOIUrl":"10.1007/s11596-026-00213-9","url":null,"abstract":"<p><p>The rising incidence of childhood metabolic disorders poses an increasingly serious public health challenge. The developmental programming of the gut microbiota during early life, shaped by perinatal and postnatal factors, establishes a functional trajectory that profoundly influences host metabolism, with microbiota-derived metabolites serving as critical bridging molecules that mechanistically link early-life exposures to metabolic outcomes in childhood. Key microbiota‒metabolite pathways underpin this process, including the fermentation of dietary fiber into short-chain fatty acids (SCFAs), the microbial metabolism of amino acids into both protective and detrimental products, the biotransformation of primary bile acids (BAs) into secondary BAs, and the generation of trimethylamine N-oxide (TMAO) from methylamine precursors. These metabolites exert their effects through diverse molecular mechanisms, spanning epigenetic regulation and receptor signaling (including farnesoid X receptor [FXR], G protein-coupled bile acid receptor 1 [TGR5], and other metabolite-sensing receptors). A deep understanding of these microbiota-derived metabolites in the context of developmental programming is therefore essential not only for advancing precise diagnosis and personalized treatment but also for informing early and targeted prevention strategies to reduce the burden of childhood metabolic diseases.</p>","PeriodicalId":10820,"journal":{"name":"Current Medical Science","volume":" ","pages":"573-587"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027794","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}