DYSF promotes monocyte activation in atherosclerotic cardiovascular disease as a DNA methylation-driven gene

Identification of DNA methylation-regulated genes as potential biomarkers for coronary heart disease via machine learning in the Framingham Heart Study

“…It has been extensively documented that DNA methylation is involved in the etiopathogenesis of CHD as a dominant epigenetic factor [ 11 – 13 ]. In addition to the previously reported enrichment of DMGs in TSS regions, CpG islands and adjacent intragenic regions [ 14 , 15 ], we noticed differences in the distribution of DMGs between TSS1500 and TSS200. There were totally 5032 and 3023 DMPs identified in TSS1500 and TSS200, respectively.…”

“…It has been extensively documented that DNA methylation is involved in the etiopathogenesis of CHD as a dominant epigenetic factor [11][12][13]. In addition to the previously reported enrichment of DMGs in TSS regions, CpG islands and adjacent intragenic regions [14,15], we Fig. 2 WGCNA and module analysis based on the training set of FHS.…”

Single cell RNA-seq resolution revealed CCR1+/SELL+/XAF+ CD14 monocytes mediated vascular endothelial cell injuries in Kawasaki disease and COVID-19

“…LMNB1 was thought to help CD14 monocyte trafficking from the endothelial barrier. And XAF1 and DYSF induced the interacted cells damages [46] , [47] , [48] , [49] , [50] , [51] . Notably, the profile of IL-1β signaling and IL-8 was related to KD [52] , [53] ; however, our findings suggest that IL-1β signaling and IL-8 are irresponsible for the share vascular lesions between KD and COV as only a few genes' expression was found to be targeted in KD and FLU and near no positive gene could be identified in COV.…”

Identification immune-related biomarkers of ankylosing spondylitis based on bioinformatics analysis

“…which is consistent with our ndings. In the past, desmoglein (DYSF) was mainly studied as one of the most common subgroups causing Dysferlinopathy [31], and a recent study [32] reported that DYSF can be used as a DNA methylation driver gene to promote monocyte activation, thereby promoting the occurrence of atherosclerotic cardiovascular disease, suggesting that transcriptional activator 3 (STAT3) may be an upstream regulator promoting DYSF. Th17 cells can secrete proin ammatory cytokines, and their differentiation is regulated by STAT3 [33].…”