Inflammation Mechanisms in Atherosclerosis Development: The Role of Immunocytokines and Adhesion Molecules

Abstract

Atherosclerosis is a progressive chronic inflammatory disease characterized by the accumulation of lipids and immune cells within the arterial wall, leading to plaque formation and vascular dysfunction. The inflammatory response plays a pivotal role in the initiation and progression of atherosclerosis, driven by complex interactions between immune cells, adhesion molecules, and immunocytokines. This review focuses on the mechanisms by which inflammation contributes to atherogenesis, emphasizing the roles of key cytokines such as tumor necrosis factor-alpha (TNF-α), interleukins (IL-1β, IL-6, IL-18), and interferon-gamma (IFN-γ). Additionally, we explore the role of adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), in facilitating monocyte recruitment and endothelial dysfunction. The interplay between oxidative stress and pro-inflammatory signaling further exacerbates plaque instability and increases the risk of cardiovascular events. Moreover, emerging data suggest that non-coding RNAs (miRNAs and lncRNAs) modulate the inflammatory response in atherosclerosis, offering potential targets for novel therapeutic interventions. Advances in RNA-based therapies, monoclonal antibodies against inflammatory mediators, and nanoparticle-mediated drug delivery present promising strategies for controlling atherosclerotic inflammation. Understanding the molecular mechanisms of inflammation in atherosclerosis will provide new insights into personalized treatment approaches aimed at reducing cardiovascular morbidity and mortality.