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N6 -methyladenosine (m6 A) modification is one of the most abundant epitranscriptomic modifications in eukaryotic mRNA, with dynamic and reversible properties. This modification process is coordinated by methyltransferases, demethylases, and related m6 A binding proteins, which in turn affect mRNA metabolism and function. Increasing evidence has indicated that the m6 A RNA modification plays an important role in the occurrence and development of atherosclerosis (As) and other related diseases. This paper provide a comprehensive review of the relationship between m6 A RNA modification and As. The entire manuscript summarizes the m6 A RNA modification mechanism and its roles in Asrelated cells including endothelial cells, macrophages, and smooth muscle cells, and discusses the association of m6 A RNA modification with risk factors of As such as high-fat diet, ischemia/hypoxia, oscillatory stress, and hypertension. Finally, this review summarizes researches on drug intervention targeting m6 A RNA methylation to mitigate As. These studies provide important references for exploring new targets for early diagnosis and treatment of As. [ABSTRACT FROM AUTHOR]

Atherosclerosis is the pathological basis of a variety of cardiovascular diseases, which are still the leading cause of human death worldwide. Ferroptosis is a kind of iron dependent non-apoptotic cell death mode, which is closely related to various physiological mechanisms. Recent studies have found that ferroptosis in macrophages plays an important role in the occurrence and development of atherosclerosis. Based on the imbalance of iron metabolism in macrophages, this paper reviews the correlation between ferroptosis in macrophages and atherosclerosis in terms of the interaction between ferroptosis in macrophages and lipid peroxidation, inflammation, oxidative stress, etc., in order to provide new ideas for the study of the pathogenesis of atherosclerosis. [ABSTRACT FROM AUTHOR]

Atherosclerosis is the main pathological basis for the occurrence and development of cardiovascular and cerebrovascular diseases. Macrophage efferocytosis deficiency exists in the formation of atherosclerosis. Defective efferocytosis leads to the accumulation of uncleared apoptotic cells and secondary necrosis, leading to characteristic formation of necrotic core and plaque instability in atherosclerosis. The complete process of efferocytosis includes recognition("find me")stage, phagocytosis("eat me")stage, and the post-processing reaction (digestion) stage. It has been reported that miRNA is involved in the regulation of key signal transduction and lipid homeostasis in atherosclerotic efferocytosis. This paper discussed the important role of efferocytosis in the process of atherosclerosis and the influence of efferocytosis defect on atherosclerosis. This review focuses on the regulatory effects of "eat me" and "don􀆳t eat me" signals of efferocytosis in the overall inflammation of atherosclerosis, and meanwhile the regulation of miRNA on lipid metabolism and inflammation regression in atherosclerosis, and the fine tuning of miRNA targeting macrophage efferocytosis in the process of atherosclerosis. [ABSTRACT FROM AUTHOR]

Macrophages play multiple roles in atherosclerosis. The progression of atherosclerosis is associated with morphological and functional changes in the lymphatic vessels of the diseased arteries, but the mechanism is not fully understood. This paper mainly reviews the origin and classification, the markers and the function of macrophage in atherosclerosis, the origin, the structure function and the markers of lymphatic vessels in atherosclerosis, the changes of arterial wall lymphangiogenesis in different stages of atherosclerotic lesions, the functional role of lymphangiogenesis in atherosclerosis, the lymphatic migration of macrophages and its mechanism involved in lymphangiogenesis, in order to provide a basis for the mechanism research and clinical treatment of atherosclerosis. [ABSTRACT FROM AUTHOR]

Circular RNA (circRNA), an emerging non-coding RNA, is closely related to the processes of lipid deposition, inflammatory response, apoptosis, proliferation and repair in atherosclerosis (As), and affects the development of As. Traditional Chinese medicine (TCM) has an important academic value in the prevention and treatment of As, and its regulatory mechanism has not been comprehensively summarized. This paper reviewed the association of circRNA with lipid deposition, inflammatory response and macrophage in As, and summarized the research progress of the correlation between circRNA and atherosclerosis and the regulation of traditional Chinese medicine. [ABSTRACT FROM AUTHOR]

Preventing the occurrence and recurrence of stroke is the top priority of the treatment strategy for ischemic cerebrovascular disease. Patients with multiple cerebral vascular stenosis and aortic arch ulcer plaques have a significantly increased risk of recurrent ischemic stroke. This paper introduces a case of probucol combined with atorvastatin in the treatment of multiple cerebral vascular stenosis with aortic arch ulcer plaque. This acute ischemic stroke patient presented with mild neurological impairment. During his hospitalization, multiple cerebral vascular stenosis and aortic arch ulcer plaques were discovered. After 3 months of sequential dual antiplatelet therapy, aspirin therapy was continued and combined with probucol and atorvastatin throughout the course for enhanced lipid-lowering antioxidant therapy. After 25 months of follow-up, there was no recurrence of stroke in this patient, and all imaging and hematological indicators remained stable. [ABSTRACT FROM AUTHOR]

Hypoxia inducible factors (HIF) are hypoxia-sensitive transcription factors that are the primary regulators of the cellular response to hypoxia. Hypoxia inducible factors induce inflammation, lipid metabolism, endothelial dysfunction, proliferation of vascular smooth muscle cells (VSMC), and regulate the development of cardiovascular diseases (CVD). This paper reviews the role of hypoxia inducible factors in CVD and the progress of the mechanism of action in recent years, and discusses the role and mechanism of hypoxia inducible factors on vascular constituent cell types and its relationship with the occurrence and development of CVD. It can provide a reference for analyzing the pathogenesis of CVD and discovering new therapeutic targets. The aim is to provide a theoretical reference for further understanding the role and mechanism of hypoxia inducible factors in the pathogenesis of CVD, and to provide a basis for the design of novel effective therapeutic agents targeting hypoxia inducible factors. [ABSTRACT FROM AUTHOR]