Association of Blood Trace Elements Levels with Cardiovascular Disease in US Adults: a Cross-Sectional Study from the National Health and Nutrition Examination Survey 2011-2016.

We aimed to explore the overall association between trace elements and cardiovascular disease (CVD) and its types in humans. A total of 5101 participants' blood samples from the 2011-2016 National Health and Nutrition Examination Survey were included. Biochemical data were collected from laboratory tests conducted at mobile screening centers. After assessing linearity, weighted logistic regression estimated the association between trace elements and various CVD types. Weighted quantile sum (WQS) regression and quantile-based g-computation (Qgcomp) evaluated the overall relationship between biological trace elements and CVD types. After fully adjusting for confounding factors, the odds ratios of overall CVD morbidity corresponding to the second, third, and fourth quartiles of higher selenium (Se) concentration were 0.711 (95% CI, 0.529-0.956, p = 0.024), 0.734 (95% CI, 0.546-0.987, p = 0.041), and 0.738 (95% CI, 0.554-0.983, p = 0.038), respectively. Moreover, an increase in the concentration of copper (Cu) was associated with an increased risk of stroke (95% CI, 1.012-1.094, p = 0.01), heart failure (95% CI, 1.001-1.095, p = 0.046), and heart attack (95% CI, 1.001-1.083, p = 0.046). As the concentration of trace elements in the body increased, there was a significant positive association between Cu and CVD prevalence. On the other hand, Se and zinc were negatively associated with CVD prevalence. A nonlinear relationship between Se and CVD was found, and an appropriate Se intake may reduce the risk of CVD. Cu levels positively correlated with CVD risk. However, prospective cohort studies are warranted to confirm the causal effects of the micronutrients on CVD and its types.

Regulatory Effects of Histone Deacetylase Inhibitors on Myeloid-Derived Suppressor Cells.

Histone deacetylase inhibitors (HDACIs) are antitumor drugs that are being developed for use in clinical settings. HDACIs enhance histone or nonhistone acetylation and promote gene transcription via epigenetic regulation. Importantly, these drugs have cytotoxic or cytostatic properties and can directly inhibit tumor cells. However, how HDACIs regulate immunocytes in the tumor microenvironment, such as myeloid-derived suppressor cells (MDSCs), has yet to be elucidated. In this review, we summarize the effects of different HDACIs on the immunosuppressive function and expansion of MDSCs based on the findings of relevant studies.

Epithelial-mesenchymal transition: When tumor cells meet myeloid-derived suppressor cells.

Myeloid-derived suppressor cells (MDSCs) are a heterogeneous myeloid cell population characterized by protumoral functions in the tumor immune network. An increasing number of studies have focused on the biological functions of MDSCs in tumor immunity. Epithelial-mesenchymal transition (EMT) is a cellular plasticity process accompanied by a loss of epithelial phenotypes and an acquisition of mesenchymal phenotypes. In general, tumor cells that undergo EMT are more likely to invade and metastasize. Recently, extensive evidence suggests that EMT is closely related to a highly immunosuppressive environment. This review will summarize the immunosuppressive capacities of MDSC subsets and their distinct role in tumor EMT and further discuss immunotherapy for tumor EMT by targeting MDSCs.