Metabolic dysfunction-associated steatotic liver disease (MASLD) impacts >30 % of the world's population, imposing significant societal and familial burdens. Arterial stiffness is a known risk factor for various metabolic disorders, and early-onset MASLD may be linked to heightened arterial stiffness. However, studies investigating the link between arterial stiffness and MASLD are limited. This study utilized data from the NHANES database, focusing on young adults aged 20 to 45 years, spanning from 2005 to 2018. The Fatty Liver Index (FLI) was used to diagnose MASLD, and the estimated Pulse Wave Velocity (ePWV) was utilized to assess arterial stiffness. The association between MASLD and arterial stiffness was analyzed using weighted multiple logistic regression models and restricted cubic splines. Sensitivity analyses were performed to evaluate the stability of the observed relationship. The study included 5 522 participants, with 3 415 serving as controls and 2 107 diagnosed with MASLD. The two groups differed significantly in age, income, and comorbidities, including hypertension and diabetes. The mean ePWV was 6.79 (SD = 0.71) in the MASLD group and 6.33 (SD = 0.57) in the control group, respectively. Adjusted weighted logistic regression models revealed that individuals in the high ePWV group (ePWV ≥ 6.559) had a 2.39-fold increased risk of onset compared to those in the low ePWV group (ePWV < 6.559), with statistical significance (P < 0.05). Restricted cubic splines (RCS) also demonstrated a positive linear correlation between ePWV and MASLD. Sensitivity analysis validated the strong correlation between ePWV and MASLD, while subgroup analysis demonstrated a positive association between ePWV and MASLD across most subgroups (OR > 1). The study indicates a strong association between arterial stiffness, as measured by ePWV, and MASLD in young adults. The results suggest that targeting arterial stiffness could aid in preventing and managing MASLD.

Introduction: The melanoma-associated antigen D2 (MAGED2) is one of the melanoma-associated antigen family members. It is commonly overexpressed in a variety of malignancies. However, the mechanism and function of MAGED2 in glioma remain unknown. Methods: The MAGED2 expression level and the correlations between clinical characteristics were analyzed with the data from the CGGA and TCGA datasets. MAGED2 expression in 98 glioma tissues was measured using RT-qPCR, Western blot, and immunohistochemistry. CCK-8, colony formation, and EdU assays were used to assess the effect of MAGED2 on U251-MG cell proliferation. Flow cytometry was used to track changes in the cell cycle and cell apoptosis following plasmid transfection with CRISPRi. Results: MAGED2 was shown to be highly expressed in glioma tissues, and high MAGED2 expression predicted poor prognosis. Furthermore, MAGED2 knockdown significantly inhibited the proliferation of U251-MG cells by preventing cell cycle arrest at the G0/G1 phase and triggering apoptosis. In line with in vitro findings, the results of the xenograft experiment and immunohistochemistry also showed that MAGED2 suppression inhibited tumor development and decreased Ki-67 expression levels. Conclusions: MAGED2 may be a possible biomarker for glioma and an important prognostic factor for glioma patients.