Atheroprotective mechanism by which folic acid regulates monocyte subsets and function through DNA methylation.

ABSTRACT:

Background

Recent studies have suggested that folic acid can restore abnormal DNA methylation and monocyte subset shifts caused by hyperhomocysteinemia (HHcy) and hyperlipidemia (HL). However, the exact mechanism of action is still not fully understood. In this study, we further investigated the reversal effect and underlying mechanism of folic acid on the shift in monocyte subsets induced by aberrant lipids and Hcy metabolism via DNA methylation in vitro and in vivo.

Results

Our results showed that intermediate monocytes were significantly increased but had the lowest global 5-methylcytosine (5-mC) levels in coronary artery disease (CAD) patients, which might lead to a decrease in the global 5-mC levels of peripheral blood leukocytes (PBLs). We also discovered that ARID5B m

SUBMITTER: Xiang Y 

PROVIDER: S-EPMC8887029 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature