Platelet Implication in Atherosclerosis Pathogenesis

Abstract

Atherosclerosis is a prevalent cardiovascular disease that leads to serious complications like myocardial infarction and ischemic stroke. Platelets play a pivotal role in thrombosis and contribute to the development of atherosclerosis through interactions with the cellular environment. Consequently, platelets have emerged as a potential therapeutic target. This review explores the normal functioning of platelets and their involvement in atherosclerosis progression, highlighting their participation in inflammatory responses within the arterial wall. Platelets activate and release mediators that promote vascular inflammation and endothelial dysfunction, key features of atherosclerotic plaque formation. They also interact with circulating immune cells, exacerbating the inflammatory milieu and fostering disease progression. Targeting platelets presents a promising approach for therapeutic interventions in atherosclerosis. Antiplatelet agents aim to impede platelet activation and aggregation, reducing thrombosis risk. Novel strategies that target platelet interactions with inflammatory cells and modulate platelet-derived inflammatory mediators are also being investigated. Further research is needed to fully exploit the potential of platelet-targeted therapy. Understanding the precise role of platelets at different stages of atherosclerosis and their interactions with immune cells and the inflammatory milieu will enhance our understanding of disease pathogenesis and guide the development of more effective therapeutic approaches. In conclusion, platelets significantly influence atherosclerosis by contributing to thrombus formation and promoting inflammatory processes. Recognizing platelets as a therapeutic target opens up new possibilities for mitigating the consequences of atherosclerosis and improving patient outcomes.