Figure 1.

Progression of ASCVD and NASH. The onset of both ASCVD and NASH begins with dysregulated lipid metabolism, leading to their accumulation in the neointimal region of the artery (fatty streak), or the hepatocytes (simple hepatic steatosis). This process enhances inflammatory pathways in both diseases. During atherosclerosis, leukocytes adhere and transmigrate into the developing plaque, where they secrete additional cytokines and chemokines (atheroma). In the liver, leukocytes from the circulation accumulate, leading to NASH (NASH without fibrosis). These immune cells secrete soluble factors to activate collagen-producing cells: synthetic vascular smooth muscle cells (vSMCs) in atherosclerosis (stable plaque), and hepatic stellate cells in the liver (NASH with fibrosis). The most advanced stages of disease are associated with higher mortality. In atherosclerosis, advanced plaques with a large necrotic core and thin fibrous caps are prone to rupture (unstable plaque), which is highly thrombogenic. In the liver, excessive fibrosis and cell death leads to irreversible damage and loss of liver function (cirrhosis).