| Summary: | Cardiovascular diseases is one of the major public health and medical concerns globally. Atherosclerosis is a condition where plaque build-up narrows the blood vessels, ultimately preventing sufficient blood flow to the heart. In current research, the role played by the human innate immune system in the development of atherosclerosis is a topic of interest. Although the specific relations require further studies, macrophages have been identified to play a key role in the progression of atherosclerosis due to their ability to mediate inflammation. Nevertheless, the mechanism that how macrophages cause inflammatory responses in atherosclerotic process and what is the risk factor that can describe the inflammation in clinic still remains unclear. This paper reviews the mechanism of macrophages to trigger inflammation and their relationships to atherosclerosis. In this study, Interferon Regulatory Factor 3 (IRF3) and its-related cytokine interleukin 1β was found to be upregulated in patients with acute coronary disease. Afterwards, the over-expressed IRF3 level and its RNA transcription was further confirmed in atherosclerotic ApoE-/-mice. Our results indicated that IRF3 was up-regulated during atherosclerotic process, which might be a potential biomarker of atherosclerosis and its-related coronary disease in clinic.
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