〔Abstract〕 Objective To explore the epicardial adipose tissue(EAT) of patients with coronary heart disease, KLF7 stimulates macrophages to secrete inflammatory factors and promotes the differentiation and maturation of adipocytes through the NF-κB signaling pathway, and to clarify the mechanism of KLF7 in the occurrence and development of CAD. Methods 30 patients with coronary heart disease(CAD group) and 30 patients without coronary heart disease(non-CAD group) were collected, and general data and biochemical indicators were collected. qRT-PCR was used to detect the expression levels of KLF7, APN, IL-6, and TNF-α mRNA in EAT. Human THP-1 cells were cultured in vitro and induced into M1 type macrophages and 3 T3-L1 preadipocytes. The cells were divided into 3 groups: KLF7 up-regulated group(transfected with KLF7 mimic), KLF7 down-regulated group(transfected with siRNA knockdown KLF7), NC group(transfected oligopeptide sequence), transfected two kinds of cells. qRT-PCR was used to detect the expression of APN, MCP-1, IL-6 and TNF-α mRNA in M1 type macrophages, and the protein expression levels of key factors in the NF-κB signaling pathway were detected by Westren blot. The qRT-PCR method was used to detect APN, KLF4, IL-6, MCP-1 mRNA and adipocyte differentiation marker peroxisome proliferator-activated receptor-γ(PPARγ) in 3 T3-L1 preadipocytes 24 h after transfection. CCAAT/enhancer binding protein α(C/EBPα), fatty acid binding protein 4(FABP4) mRNA relative expression levels, and Westren blot was used to detect protein expression levels. Results Compared with the non-CAD group, the expression of CAD group decreased, APN decreased, IL-6 and TNF-α increased significantly, and the difference was statistically significant(P<0.01). KLF7 was highly expressed in human THP-1 derived M1 macrophages induced by inflammatory stimuli(LPS). In M1 macrophages derived from human THP-1, knocking down KLF7 could inhibit the release of inflammatory factors. Transfection with KLF7-siRNA could significantly inhibit LPS-induced phosphorylation of JNK-MAPKs, the level of p-p65 and the activation of p-IκBa(P<0.05). In 3 T3-L1 preadipocytes, upregulation of KLF7 increased the expression of adipocyte differentiation markers PPARγ, C/EBPa, FABP4 mRNA, and promoted the differentiation of 3 T3-L1 preadipocytes into adipocytes(P<0.05). Conclusion The expression of KLF7 in EAT in CAD patients increases. KLF7 activates the activation of macrophages mediated by the JNK-NF-KB signaling pathway in EAT, promotes inflammation in EAT in CAD patients, and promotes the differentiation and maturation of adipocytes, thereby promoting the development of CAD. It indicates that KLF7 may be a potential therapeutic target for cardiovascular diseases(such as CAD).