Fig. 3: Schematic diagram of the mechanism by which cellular senescence functions in the progression of atherosclerosis.
From: The role of cellular senescence in cardiovascular disease
The left side shows a cross-section of an arterial vessel. In the intima, there is infiltration of immune cells such as monocytes, lymphocytes, and neutrophils, along with endothelial dysfunction. Smooth muscle cells (SMCs) exhibit abnormal proliferation and secrete collagen and fragments. Additionally, there is an inflammatory response and accumulation of M1 macrophages. The right side presents a local magnification and further mechanistic details. Senescent endothelial cells undergo cell cycle arrest (Cell cycle arrest, p16,p21) and secrete the senescence-associated secretory phenotype (SASP, including IL-6, IL-1β, MMPs), leading to cell death, foam cell formation, macrophage activation, It also involves structural changes in the fibrous cap (FIBROUS CAP) and pathological alterations in various layers of the vessel wall (including the intima, internal elastic lamina, and media), ultimately promoting the development and progression of atherosclerosis.
