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Atherosclerosis (AS) is a chronic inflammatory disease. Unstable atherosclerotic plaque rupture, vascular stenosis, or occlusion caused by platelet aggregation and thrombosis lead to acute cardiovascular disease. The main lesions in atherosclerosis are characterized by lipid deposition in parts of the artery accompanied by smooth muscle cell and fibrous matrix proliferation, which gradually develop into the formation of an atherosclerotic plaque. Atherosclerosis is usually considered a chronic inflammatory disease as inflammation plays an important role in all stages of the atherosclerotic process. Cell death, an inevitable destiny of all life, is crucial to organismal homeostasis. When it is dysregulated, this will lead to a series of pathological consequences. Regulated cell death relies on specialized molecular machinery and differs from classic necrosis that is unregulated cell death caused by overwhelming physical, chemical, or biological insults. Programmed cell death as a subset of regulated cell death includes classical apoptosis in the context of development and tissue homeostasis, and other forms that occur in the microenvironment of exogenous or endogenous perturbations, such as necroptosis, pyroptosis, autophagy, ferroptosis. Different cell death pathways are interrelated at multiple levels and have special effects on the development of AS. Thus, the aim of the project is to further investigate the mechanisms of cell death and its role in AS.