Figure 1.

The interplay of ATF3 with metabolism on inflammation. HDL mediates anti-inflammatory reprogramming of macrophages via ATF3 in macrophages, but also induced ATF3 activity in endothelial cells then promote inflammation. ATF3 regulates Clec4e signaling to increase cholesterol efflux and reduce ER stress and inflammation. TL increases nuclear ATF3 accumulation. The accumulation of ATF3 can down-regulate TNF signaling and alleviate inflammation and apoptosis. ATF3 can also increases lipolysis, which exacerbates apoptosis and inflammation in carotid artery endothelial cells in the cerebrovascular system.

ATF3: activating transcription factor 3; HDL: high-density lipoprotein; TLR: toll-like receptor; Clec4e: c-type lectin receptor 4e; ER: endoplasmic reticulum; TL: Triglyceride; TNF: tumor necrosis factor.