The SASP from senescent cells exerts many pro-atherogenic effects, which may involve vascular remodelling, plaque formation and rupture. Notably, there is evidence that the SASP, as a source of chronic inflammation and some plaque instability factors, is involved in the pathogenesis and development of atherosclerosis. They can also establish the SASP, which can cause increased secretion of various inflammatory cell cytokines, chemokines and matrix-degrading proteases. Senescent cells from atherosclerotic plaques are lack proliferation, overexpress P16INK4A, P53, P21, and increase the activity of senescence-associated beta-galactosidase (SAОІG). Cell senescen ce and atherosclerosis have multiple common aetiological stimuli, but senescent cells are not just simple bystanders. Atherosclerosis is considered a chronic inflammatory disease, and atherosclerotic plaques present with cell senescence. Recent clinical trials have clearly demonstrated a causal relationship between inflammation and human atherosclerosis. Furthermore, a variety of molecules involved in the SASP can serve as promoters and biomarkers of cardiovascular diseases including atherosclerosis. Moreover, the SASP can also induce the enlargement of local and systemic senescence to neighbouring cells via paracrine or endocrine mechanisms. The SASP contributes to the secretion of inflammatory cell cytokines and chemokines that induce local and systemic inflammatory responses, immune system activation, tissue damage and fibrosis, and cell apoptosis and dysfunction. One of the mechanisms is cell senescence, which can lead to chronic inflammation through the SASP. Because ageing is a modifiable factor, it can be viable to slow down the development of age-related diseases by regulating basic ageing mechanisms. At the same time, increasing evidence suggests that ageing is one of the greatest risk factors for atherosclerosis. It is well known that there are many different risk factors for atherosclerosis such as high blood pressure, low-density lipoprotein (LDL) cholesterol, diabetes and smoking. Atherosclerosis as a chronic inflammatory disease of the blood vessel walls is the main potential cause of CVD. This review systematically summarizes the multiple roles of the SASP in atherosclerosis and can contribute to the exploration of new therapeutic opportunities.ДЄgeing has long been considered a major risk factor for many chronic and fatal diseases, including cardiovascular diseases (CVDs), neurodegenerative diseases and cancer. Finally, we focus on a variety of novel therapeutic strategies aimed to reduce the burden of atherosclerosis in elderly individuals by targeting senescent cells and inhibiting the regulatory mechanisms of the SASP. Furthermore, the SASP can deliver senescence signals to the surrounding vascular cells, gradually contributing to the development of atherosclerosis. As a significant mediator of the harmful effects of senescent cells, it can play a pro-atherogenic role by producing inflammation and immune dysfunction. The SASP from different types of senescent cells have vital roles in atherosclerosis progression.

Importantly, we provide novel perspectives on how the SASP can promote atherosclerosis. In this review, we concretely describe the characteristics of the SASP and its regulation mechanisms. As a vital marker of cellular senescence, the senescence-associated secretory phenotype (SASP) is a novel mechanism to link cellular senescence with atherosclerosis. Abnormal accumulation of senescent cells can cause potentially deleterious effects on the organism with age. The global population of older individuals is growing, and ageing is a key risk factor for atherosclerotic cardiovascular diseases.

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