HISTOPATHOLOGICAL AND MOLECULAR MECHANISMS OF ATHEROSCLEROSIS DEVELOPMENT AND PROGRESSION

Atherosclerosis is a chronic inflammatory disease of medium-sized and large arteries characterized by lipid accumulation, endothelial dysfunction, inflammatory cell infiltration, and progressive structural remodeling of the vascular wall. The development of atherosclerotic lesions involves complex interactions between circulating lipoproteins, vascular endothelial cells, smooth muscle cells, macrophages, and extracellular matrix components. This article examines the histopathological and molecular mechanisms underlying the initiation, progression, and complications of atherosclerosis. Particular attention is devoted to endothelial dysfunction, low-density lipoprotein retention and modification, foam cell formation, vascular smooth muscle cell phenotypic changes, and fibrous plaque development. The study is based on a narrative analysis of established scientific literature using descriptive, comparative, and morphological-functional approaches. The findings indicate that atherosclerosis is not simply a consequence of lipid deposition but represents a dynamic inflammatory and fibroproliferative process. Plaque vulnerability is influenced by the composition of the fibrous cap, inflammatory activity, lipid-rich necrotic core, and local vascular conditions. Understanding the cellular and histological mechanisms of atherosclerosis is essential for improving cardiovascular risk assessment, prevention, and therapeutic strategies.