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Abstract Metabolic dysfunction-associated steatotic liver disease (MASLD) brings heavy clinical and economic burdens to patients worldwide. High fasting plasma glucose (HFPG) was proven to be an important modifiable risk factor. However, the global burden distribution of HFPG-attributable MASLD has not been fully studied. This study aimed to describe the epidemiological distribution and trends of the burden of HFPG-attributable MASLD worldwide. The data source was the 2021 Global Burden of Disease Study. Descriptive statistics were mainly conducted using disability-adjusted life years (DALYs) and deaths of HFPG-attributable MASLD from 1990 to 2021, as well as their age-standardized rates (ASRs) and population-attributable fractions. Subgroup analyses were conducted by region, age group, and sex. We found that 213.48 thousand DALYs and 10.02 thousand deaths in MASLD were attributable to HFPG worldwide in 2021, with an increase of 2.96 and 3.32 times compared with 1990, respectively. Over the past 32 years, age-standardized DALY rates (ASDRs) have fluctuated upward, reaching 2.45 per 100,000 people in 2021, with an increase of 81.21%. The ASDRs continued to rise in low, low-middle, and high social demographic index (SDI) regions, fluctuated upward at high levels in middle SDI regions, and were relatively low in high-middle SDI regions. People aged 50–69 accounted for the largest proportion of DALYs, while people over 70 had the largest increase of 3.73 times. Men had higher ASDRs, and the sex difference has been gradually expanding over the past 32 years, peaking at the age of 45–49. In conclusion, the burden of HFPG-attributable MASLD has continued to increase globally, with differences in geographical area, age, and sex distribution. HFPG, as a modifiable risk factor, should be given more importance. The implementation of targeted health intervention strategies is recommended for each country based on trends in the burden of HFPG-attributable MASLD.

Objectives: To investigate PI3K-Akt-mTOR signaling pathway changes and the proliferation of FoxP3+Treg cells in patients with active tuberculosis. Methods: We isolated PBMCs and CD4+CD25+FoxP3+Treg cells from peripheral blood collected from patients with active tuberculosis and healthy controls. We compared the proportion and MFI of PI3K-Akt-mTOR pathway components and PTEN by flow cytometry using specific cell-surface and intracellular markers. Moreover, we detected the specific secretory proteins ESAT-6 and Ag85B, cytokines IL-10, TGF-β1 and IL-35 in serum by ELISA. Results: Compared with healthy controls, the proportions of CD3+Akt+, CD3+p-Akt+, CD3+mTOR+, CD3+p-mTOR+ and CD3+PTEN+ cells, in the T lymphocyte population of patients with active tuberculosis, were decreased (p

MicroRNA (miR)-590 has been established to be a promoter of cell proliferation, migration and invasion, and an inhibitor of apoptosis in numerous cancer cell lines. However, its effects on non-cancer cells remain to be elucidated. miR-590 was transfected into human umbilical cord mesenchymal stem cells (HUMSCs), and the cell proliferation rate was determined using a Cell-Light 5-ethynyl-20-deoxyuridine Apollo 567 kit and the presence of extracellular matrix (ECM) proteins were detected using western blot analysis and immunofluorescence microscopy. Using bioinformatic analysis and dual-luciferase assays, the novel target miR-590 was identified. In addition, the effects of miR-590 on cell proliferation and ECM enhancement were also evaluated. The results of the present study demonstrated that miR-590 interacts directly with the 3'-untranslated region of Mothers Against Decapentaplegic Homolog 7 (Smad7), which is an important factor in transforming growth factor-ß signaling pathway. Overexpression of miR-590 downregulated Smad7 expression at the mRNA and protein level, and subsequently resulted in cell proliferation and ECM accumulation. Additionally, the transfection of small interfering RNA targeting Smad7 in HUMSCs produced similar effects on cell proliferation and ECM to the overexpression of miR-590. The results of the present study indicated that miR-590 affects HUMSC proliferation by directly targeting Smad7. [ABSTRACT FROM AUTHOR]