Modulation of cardiac resident macrophages immunometabolism upon high-fat-diet feeding in mice

• DOI: 10.3389/fimmu.2024.1371477
• Publication Date: 2024-06-28T04:26:36Z
• Authors: Simeng Zhu; Yujia Liu; Guofang Xia; Xiaoqing Wang; Ailian Du; Jin Wu; Yanpeng Wang; Yuanlong Wang; Chengxing Shen; Peng Wei; Congfeng Xu
• Keywords: Cardiac Fibrosis; Pathophysiology

Background A high-fat diet (HFD) contributes to various metabolic disorders and obesity, which are major contributors cardiovascular disease. As an essential regulator for heart homeostasis, cardiac resident macrophages may go awry contribute pathophysiology upon HFD. Thus, better understand how HFD induced dysfunction, this study intends explore the transcriptional functional changes in of mice. Methods C57BL/6J female mice that were 6 weeks old fed with or normal chow (NCD) 16 weeks. After evaluation functions by echocardiography, mouse hearts harvested CCR2 - sorted, followed Smart sequencing. Bioinformatics analysis including GO, KEGG, GSEA analyses employed elucidate changes. Results Hyperlipidemia obesity observed easily The also displayed more severe fibrosis diastolic dysfunction sequencing revealed dysfunctions, especially lipid-related genes pathways. Besides this, antigen-presentation-related gene such as Ctsf inflammation, particularly NF-κB signaling complement cascades, underwent drastic macrophages. GO cellular compartment was performed showed specific organelle enrichment trends involved genes. Conclusion Dysregulated metabolism intertwines inflammation feeding mice, further research on crosstalk among organelles could shed light potential mechanisms.