Neurodegenerative diseases (NDs) represent a major global health challenge in aging populations, with their incidence continuing to rise worldwide. Although substantial progress has been made in elucidating the clinical features and molecular underpinnings of these disorders, the precise mechanisms driving neurodegeneration remain incompletely understood. This review examines the increasing significance of the gut–brain–immune triad in the pathogenesis of NDs, with particular attention to Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and multiple sclerosis. It explores how disruptions in gut microbiota composition and function influence neuroinflammation, blood–brain barrier integrity, and immune modulation through microbial-derived metabolites, including short-chain fatty acids, lipopolysaccharides, and bacterial amyloids. In both Alzheimer’s and Parkinson’s diseases, a reduced abundance of short-chain fatty acid-producing bacterial taxa has been consistently associated with heightened pro-inflammatory signaling, thereby facilitating disease progression. Although detailed mechanistic understanding remains limited, experimental evidence—primarily from rodent models—indicates that microbial metabolites derived from a dysbiotic gut may initiate or aggravate central nervous system dysfunctions, such as neuroinflammation, synaptic dysregulation, neuronal degeneration, and disruptions in neurotransmitter signaling via vagal, humoral, and immune-mediated pathways. The review further highlights how gut microbiota alterations in amyotrophic lateral sclerosis and multiple sclerosis contribute to dysregulated T cell polarization, glial cell activation, and central nervous system inflammation, implicating microbial factors in disease pathophysiology. In addition to identifying critical knowledge gaps, the review emphasizes the need for sustained, multifactorial research efforts, including the development of physiologically relevant brain–gut organoid models and the implementation of standardized experimental protocols. A major limitation in the field remains the difficulty of establishing causality, as clinical manifestations often arise after extended preclinical phases—lasting years or decades—during which aging, dietary patterns, pharmacological exposures, environmental factors, and comorbidities collectively modulate the gut microbiome. Finally, the review discusses how microbial influences on host epigenetic regulation may offer innovative avenues for modulating neuroimmune dynamics, underscoring the therapeutic potential of targeted microbiome-based interventions in neurodegenerative diseases.

Drug-induced liver injury (DILI) represents a prevalent adverse event associated with medication use. However, the exact mechanisms underlying DILI remain incompletely understood, and the lack of specific diagnostic and prognostic biomarkers poses significant challenges to the clinical diagnosis and treatment of this condition. Consequently, our study aimed to endeavor to identify serum and fecal metabolic biomarkers, enabling more accurate DILI diagnosis and improved prediction of chronic progression.

Untargeted metabolomics analysis was performed on serum and fecal samples obtained from a cohort of 32 DILI patients (causality confirmed via the updated Roussel Uclaf Causality Assessment Method) and 36 healthy controls. Utilizing techniques such as partial least squares-discriminant analysis modeling and t-tests, we identified significantly differentially expressed metabolites and metabolite sets. Causality assessment was performed using the updated Roussel Uclaf Causality Assessment Method.

The findings from the analysis of serum and fecal metabolomics association pathways suggested that perturbations in bile acid metabolism might serve as potential mechanisms underlying the progression of DILI. Our study revealed 22 overlapping differential metabolites between serum and feces, displaying significant concentration differences between the DILI and healthy control groups. Notably, we identified chenodeoxycholic acid and deoxycholic acid as promising markers that not only distinguished DILI patients from healthy individuals but also exhibited predictive potential for DILI chronicity.

The integrated analysis of serum and fecal metabolites uncovers the significant disruption of bile acid metabolites as a key contributing factor in the pathogenesis of DILI. Our study offers promising potential biomarkers for the diagnosis and prognosis of DILI, paving the way for a novel perspective in the realm of DILI diagnosis and treatment.

General transcription factor IIIC subunit 2 (GTF3C2) is one of the polymerase III transcription-related factors. Previous studies have revealed that GTF3C2 is involved in regulating cell proliferation. However, the role of GTF3C2 in hepatocellular carcinoma (HCC) remains unclear. This study aimed to determine its expression, biological function, and mechanism in HCC.

The expression of GTF3C2 in HCC and non-tumor tissues, along with its clinical significance, was investigated using public databases and clinical samples. Reverse transcription-quantitative polymerase chain reaction and Western blot assays were performed to detect the expression of GTF3C2, ubiquitin specific peptidase 21 (USP21), mitogen-activated protein kinase 2 (MEK2), extracellular signal-regulated kinase 1/2 (ERK1/2), and p-ERK1/2 in cells. A luciferase reporter assay was conducted to explore the regulatory effect of GTF3C2 on USP21 transcription. Cell Counting Kit-8, 5-ethynyl-2′-deoxyuridine, and colony formation assays were performed to assess HCC cell proliferation. Subcutaneous injection of HCC cells into nude mice was used to evaluate tumor growth in vivo.

GTF3C2 expression was upregulated in HCC tissues and was positively correlated with advanced tumor stages and high tumor grades. HCC patients with high GTF3C2 expression had significantly worse survival outcomes. Knockdown of GTF3C2 suppressed the proliferation of Hep3B and HCCLM3 cells, while overexpression of GTF3C2 facilitated the proliferation of SNU449 and Huh7 cells. GTF3C2 promoted USP21 expression by activating its transcription, which subsequently increased the levels of MEK2 and p-ERK1/2 in HCC cells. Overexpression of both USP21 and MEK2 counteracted the GTF3C2 knockdown-induced inactivation of the ERK1/2 pathway. Moreover, GTF3C2 promoted HCC cell proliferation in vitro and tumor growth in vivo by regulating the USP21/MEK2/ERK1/2 pathway.

Upregulation of GTF3C2 is frequently observed in HCC tissues and predicts poor prognosis. GTF3C2 promotes HCC cell proliferation via the USP21/MEK2/ERK1/2 pathway.

This review presents the latest evidence on the link between genetic single nucleotide polymorphisms and dental caries, highlighting key genes and pathways involved, introducing foundational concepts, and discussing essential methodological considerations for future research. Several genes have been identified as significantly associated with caries experience, including those related to tooth mineral tissues, taste perception, salivary composition and flow, and immune response. Epistatic interactions appear to be crucial in explaining genetic influence. Inconsistencies in the literature are attributed to variations in caries classification, age groups, ethnic backgrounds, limited statistical power, and linkage disequilibrium. Population stratification often confounds results, and few studies adequately control for genetic ancestry. Ensuring Hardy-Weinberg equilibrium and accounting for linkage disequilibrium are essential to avoid bias. Bonferroni corrections for multiple comparisons are fundamental but rarely applied, contributing to inconsistent findings. In conclusion, genetic epidemiology studies suggest that dental caries has a genetic component, accounting for significant individual differences in disease risk.

Wilms tumor is the most common kidney tumor in children aged 0-14 years. MicroRNAs are small, noncoding RNAs linked to the development of malignant tumors. Several studies have shown the association between single nucleotide polymorphism in miR-27a and cancer risk. This study aimed to explore the potential impact of the miR-27a rs895819 T>C polymorphism on Wilms tumor susceptibility.

The rs895819 T>C polymorphism was genotyped using the TaqMan method in 145 patients with Wilms tumors and 531 controls. Logistic regression models were used to assess the association between this polymorphism and Wilms tumor risk. A stratified analysis was also performed based on age, sex, and clinical stage.

The rs895819 T>C polymorphism showed genotypic distribution consistent with Hardy-Weinberg equilibrium (P = 0.749). The differences were not statistically significant. The miR-27a rs895819 T>C polymorphism was not significantly associated with Wilms tumor susceptibility, and the stratified analysis did not yield any significant differences.

Our study provides evidence of a lack of association between the miR-27a rs895819 T>C polymorphism and Wilms tumor susceptibility. Further validation through larger sample sizes and additional genetic polymorphisms is warranted.

With the widespread application of systemic treatments for hepatocellular carcinoma, liver injury caused by molecular targeted drugs and immune checkpoint inhibitors has become a common clinical problem. The Chinese Society of Hepatology, Chinese Medical Association, organized domestic experts to summarize and analyze adverse liver reactions, as well as advances in the diagnosis and treatment related to systemic therapy for liver cancer, both domestically and internationally. Based on this work, we formulated the “Consensus on the Management of Liver Injury Associated with Targeted Drugs and Immune Checkpoint Inhibitors for Hepatocellular Carcinoma”, aiming to provide practical recommendations and decision-making guidance for clinicians in hepatology and related specialties. This guidance focuses on the monitoring, diagnosis, prevention, and treatment of liver injury during targeted and immune checkpoint inhibitor therapy, ultimately helping more liver cancer patients benefit from targeted immunotherapy.

Prostate cancer is the second most diagnosed cancer in men worldwide and a significant cause of cancer-related death. Proteogenomic analysis offers insights into how genomic mutations influence protein expression and can identify novel biomarkers. This study aimed to investigate the impact of missense mutations on protein abundance in prostate cancer versus healthy tissues using SILAC-based quantitative proteomics.

Mass spectrometry data from prostate tumors and adjacent healthy tissues were analyzed using stable isotope labeling. Peptides were classified based on their abundance into RefSeq and Variant Abundant groups. Missense mutations were mapped via RefSeq and dbPepVar databases. Protein intensity metrics were compared, and Spearman’s correlation was used to evaluate the relationship between mutation presence and protein abundance.

Functional enrichment revealed that RefSeq Abundant proteins are involved in normal metabolic and structural functions, while Variant Abundant proteins are enriched in tumor-related pathways such as immune evasion and apoptosis suppression. A significant negative correlation was found between protein intensity difference and ratio (p < 0.05), indicating that missense mutations contribute to altered protein expression. Mutation hotspot analysis identified recurrent alterations in genes such as PPIF and ACTB. PROVEAN was used to evaluate the functional impact of variants, identifying several as deleterious to protein stability and function.

Missense mutations are associated with altered protein abundance and may promote oncogenic processes in prostate cancer. These findings enhance the understanding of genome-proteome interactions and could support the development of targeted biomarkers and therapies.