Abstract
Platelet hyperactivity leads to thrombosis, the primary cause of cardiovascular and cerebrovascular adverse events. Emerging evidence suggests that autophagy plays a fundamental role in platelet function, both at baseline and in response to stress. Autophagy is an intracellular mechanism devoted to the removal and recycling of damaged cytoplasmic cargoes. Basal level of autophagy ensures physiological platelet aggregation and hemostasis. Autophagy is impaired in platelets isolated from subjects at high cardiovascular risk whereas autophagy stimulation reduces platelet hyperactivity, along with an overall amelioration of oxidative stress status. In this mini-review, we explore the current literature on the role of autophagy in platelet biology and its relevance as a therapeutic target for counteracting cardiovascular diseases.