Thrombosis in the context of atherosclerosis typically results in life-threatening consequences, including acute coronary events and ischemic stroke. As such, early detection and treatment of thrombosis in atherosclerosis patients is essential. Clinical diagnosis of thrombosis in these patients is typically based upon a combination of imaging approaches. However, conventional imaging modalities primarily focus on assessing the anatomical structure and physiological function, severely constraining their ability to detect early thrombus formation or the processes underlying such pathology. Recently, however, novel molecular and non-molecular imaging strategies have been developed to assess thrombus composition and activity at the molecular and cellular levels more accurately. These approaches have been successfully used to markedly reduce rates of atherothrombotic events in patients suffering from acute coronary syndrome (ACS) by facilitating simultaneous diagnosis and personalized treatment of thrombosis. Moreover, these modalities allow monitoring of plaque condition for preventing plaque rupture and associated adverse cardiovascular events in such patients. Sustained developments in molecular and non-molecular imaging technologies have enabled the increasingly specific and sensitive diagnosis of atherothrombosis in animal studies and clinical settings, making these technologies invaluable to patients' health in the future. In the present review, we discuss current progress regarding the non-molecular and molecular imaging of thrombosis in different animal studies and atherosclerotic patients.

Atherosclerosis is a common problem in healthy people around the world. Long noncoding RNAs (lncRNAs) play important roles in atherosclerosis. Myocardial infarction‐associated transcript (Miat) is a cardiovascular disease‐associated lncRNA. Its role and mechanism in atherosclerosis is still not fully clarified. Our study aims to explore the role and mechanism of lncRNA Miat in atherosclerosis. The atherosclerosis models were established both in vitro and in vivo. Real‐time PCR was used to measure the expression of lncRNA Miat, miR‐214, Caspase‐1 and IL‐1β. Western blot was performed to detect the protein expression of Caspase‐1. CCK‐8 assay, Tunel staining, and flow cytometry analysis were conducted to detect proliferation and apoptosis of human aortic endothelial cells (HAECs), respectively. Oil red O staining and HE staining were used to evaluated the histological changes of the aorta. The results found that lncRNA Miat was upregulated in ox‐LDL‐induced atherosclerosis model in vitro. The inhibition of lncRNA Miat protects against ox‐LDL‐induced HAEC injury, presented as increased cell viability and decreased apoptosis. LncRNA Miat and miR‐214 has binding site, and CASP1, which encodes Caspase‐1, is a target of miR‐214. The downregulation of lncRNA Miat increased the expression of miR‐214‐3p and decreased the expression of Caspase‐1, as well as its downstream molecule IL‐1β in HAECs. However, the inhibition of miR‐214‐3p attenuated the effect of lncRNA Miat downregulation on HAECs. Furthermore, the downregulation of lncRNA Miat alleviated atherosclerosis in ApoE‐deficient mice. Correspondingly, the expression of miR‐214‐3p was upregulated and Caspase‐1 was downregulated after knockdown of lncRNA Miat. In conclusion, downregulation of lncRNA Miat exerts a protective effect against atherosclerosis through the regulation miR‐214‐3p/Caspase‐1 signalling pathway. Therefore, the inhibition of lncRNA Miat expression may be an effective strategy in the treatment of atherosclerosis.