Background: Chronic kidney disease (CKD) is a progressive condition affecting over 10% of the global population, with high sodium intake identified as a critical modifiable risk factor. This study investigated the global burden of CKD due to excessive sodium intake in 204 countries and territories from 1990 to 2021 and made the first future projections to 2040, addressing gaps in longitudinal analysis of sodium-related CKD trends and demographic differences.Methods: Data from the Global Burden of Disease (GBD) 2021 database were analyzed to quantify CKD-related deaths and disability-adjusted life years (DALYs) linked to high sodium intake. Age-standardized mortality rates (ASMR) and DALY rates (ASDR), alongside the sociodemographic index (SDI), were used to assess regional and demographic variations. Statistical analyses in R included joinpoint regression to identify temporal inflection points and age-period-cohort (APC) modeling to disentangle age, period, and birth cohort effects. Future projections show that from 2021 to 2040, the global ASMR trend is stabilizing and ASDR is on the rise. Moreover, male ASMR and ASDR have been consistently higher than female ASMR. This gender difference is expected to continue for a long time, with men continuing to bear a greater burden of chronic kidney disease than women.Results: Between 1990 and 2021, global CKD deaths attributed to high sodium intake surged 1.68-fold (26,072 to 69,954), while DALYs increased by 135% (741,197 to 1,705,325). ASMR and ASDR rose markedly in high-income regions (20.73% and 6.77%, respectively), with Latin America and the Caribbean reporting the highest burdens (ASMR: 1.49/100,000; ASDR: 33.21/100,000). Men exhibited consistently higher burdens than women, peaking in the 65–79 age group. Low SDI regions showed declining trends, contrasting with widening inequalities in medium SDI areas.Conclusion: The global CKD burden attributable to high sodium intake has escalated dramatically over three decades, driven by aging populations, dietary shifts, and regional disparities. Urgent, targeted interventions—such as sodium reduction policies, gender-specific health strategies, and enhanced healthcare access—are critical to curbing this trend, particularly in high-risk demographics and high-income regions.

Background: High body mass index (BMI) is a key metabolic risk for liver cancer, yet global assessments of its impact are limited. This study analyzes the liver cancer burden linked to high BMI from 1990 to 2021, using frontier analysis to evaluate prevention efficiency at different SDI levels and providing future predictions of the global burden up to 2040 to guide public health strategies. Method: We analyzed global burden mortality and disability rates using 2021 data, applying age-period-cohort modeling to assess the temporal dynamics of BMI-related liver cancer burden, adjusting for period and cohort effects across 204 countries and 21 regions, stratified by sex, age, and Sociodemographic Index (SDI). The analysis incorporated frontier efficiency estimates to understand the best achievable burden reduction at each SDI level and utilized a Bayesian framework for future trend predictions. Result: From 1990 to 2021, high BMI-related liver cancer deaths reached 46,200.88 worldwide, predominantly affecting men, especially ages 70–74 and 60–64 for DALYs. The disease burden varies nonlinearly with SDI, with regional disparities: Southeastern South America and Central/Eastern Europe face the highest impact, despite higher SDIs in Japan, South Korea, and Singapore, where the burden is comparatively lower. Frontier analysis reveals that countries with higher SDI levels have optimized prevention and control strategies, achieving lower burdens, while lower SDI regions still face significant challenges. The future projections indicate that the global burden of high BMI-related liver cancer will continue to rise by 2040, with rapid increases in male populations, although female predictions show more gradual growth. Conclusion: High BMI contributes to the increasing and unequal global burden of liver cancer, mainly impacting men, seniors, and middle-to-high SDI areas. Urgent, targeted efforts are needed to combat obesity, metabolic issues, and healthcare inequalities to reduce future risks. Future prevention strategies should incorporate continuous monitoring and adaptive responses to dynamic factors influencing liver cancer attributable to high BMI.

Objectives: Vacuolar protein sorting-associated protein VTA1 homolog (VTA1) encodes a factor involved in multivesicular body trafficking. This investigation sought to determine if VTA1 might function as a diagnostic indicator, a standalone prognostic element, and a potential therapeutic target in breast cancer. Methods: We performed a pan-cancer analysis of VTA1 expression using TCGA data from 33 cancer types and assessed immune infiltration with TIMER2.0. Breast cancer data from TCGA and Gene Expression Omnibus (GEO) database were collected to complete the difference analysis, clinical feature correlation, prognosis analysis, enrichment analysis, and tumor microenvironment score analysis of VTA1 in BRCA. The presence of VTA1 in BRCA cells was verified by Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR), Western Blot (WB), and Immunohistochemistry (IHC). Results: VTA1 expression was markedly elevated in breast cancer. Elevated levels were significantly linked to worse overall survival (OS). (hazard ratio [HR] = 1.791, 95 % CI: 1.206–2.659, p<0.01) and recurrence-free survival (RFS), indicating that VTA1 is an independent prognostic factor. In the tumor immune microenvironment, high VTA1 expression correlated with increased infiltration of myeloid and resting immune cells but decreased effector/activated immune cells, suggesting poor prognosis. Conclusions: VTA1 is a promising prognostic indicator for various cancers, particularly in breast cancer. The expression of VTA1 is markedly elevated in breast cancer tissues relative to the adjacent normal tissues. Clinical analyses further suggest that VTA1 functions as an independent indicator associated with unfavorable outcomes in breast cancer. These findings imply that VTA1 may serve as a promising biomarker for diagnosis, therapeutic guidance, and survival prediction.

Background: Glutamine metabolic reprogramming is a hallmark of tumor progression and is highly correlated with poor clinical outcomes. The excessive uptake of glutamine by tumor cells is a key factor contributing to widespread invasion, metastasis, and immune suppression. SLC38A2, an amino acid transporter widely expressed on the surface of tumor cells, has not been thoroughly studied regarding its function and prognostic significance in tumor progression. Our objective is to employ bioinformatics methods to conduct a comprehensive and in-depth analysis of SLC38A2 across various cancers, aiming to elucidate its role and prognostic value in tumor biology.Methods: By comprehensively incorporating gene expression and clinical data from the TCGA tumor database, GTEx database, Human Protein Atlas, and GEO database, we analyzed the expression profile, mutations, and established prognostic models for SLC38A2 across various cancers. Additionally, we investigated the enrichment of SLC38A2 at the single-cell level in 12 types of cancer and analyzed its temporal expression patterns in different cell subgroups in breast and pancreatic cancer. We also studied the correlation between SLC38A2 and glutathione metabolism.Results: Compared to normal tissues, SLC38A2 exhibits significant differential expression in 15 types of cancer and serves as a prognostic risk factor in BRCA (HR = 1.597, p < 0.05), LUAD (HR = 1.650, p < 0.01), MESO (HR = 2.007, p < 0.05), and PAAD (HR = 1.761, p < 0.05), while acting as a protective factor in KIRC (HR = 0.625, p < 0.05). Furthermore, SLC38A2 is positively correlated with tumor and stromal cells, negatively correlated with immune cell infiltration, and associated with immune exhaustion. In BRCA, SLC38A2 is highly expressed during early differentiation of malignant and stromal cells, and enriched in late differentiation of immune cells. Moreover, the expression of SLC38A2 shows a general positive correlation with glutathione metabolism genes in BRCA, LUAD, MESO, and PAAD, demonstrating diagnostic value.Conclusion: SLC38A2 shows widespread changes in expression patterns within tumor tissues, making it an effective diagnostic and prognostic biomarker. It is enriched in malignant cells and tumor-infiltrating stromal cells, while negatively correlated with the infiltration of many cells involved in anti-tumor immunity. Targeting SLC38A2 presents a viable therapeutic strategy by inhibiting glutamine competition and relieving immune suppression in the tumor microenvironment.