Zhiqiang Huang

TL;DR: It is demonstrated that a co-repressor complex containing G protein pathway suppressor 2 (GPS2) crucially controls the macrophage epigenome during activation by metabolic stress and links co- Repressor-dependent epigenomic alterations in macrophages to AT inflammation and the development of T2D.

TL;DR: It is shown that GPS2 inhibits PPARα activity and that ablation of GPS2 ameliorates hepatic steatosis in mice, suggesting that the GPS2-PPARα partnership in hepatocytes coordinates the progression of NAFLD in mice and in humans and thus might be of therapeutic interest.

TL;DR: It is demonstrated that adipocyte hypertrophy is triggered by loss of the corepressor GPS2 during obesity, and proposed that the obesity-associated loss of GPS2 in adipocytes predisposes for a maladaptive WAT expansion and a pro-diabetic status in mice and humans.

TL;DR: This work will highlight macrophage pathways that are controlled by multifaceted repression events, along with a discussion of underlying regulatory mechanisms and components, and emphasize how alterations of macrophages repression pathways in humans contribute to, or even cause, metabolic inflammatory diseases such as obesity and type 2 diabetes.

TL;DR: In this paper, a corepressor-eRNA-chemokine pathway was investigated using inflammatory macrophage activation as a model, and corepressors co-occupy candidate enhancers along with the coactivators CBP (H3K27 acetylase) and MED1 (mediator) but act antagonistically by repressing eRNA transcription-coupled H3K 27 acetylation.