Role of platelets as mediators that link inflammation and thrombosis in atherosclerosis

Abstract

Platelets, crucial mediators of the acute complications of atherosclerosis that cause life-threatening ischemic events at late stages of the disease, are also key effectors of inflammation throughout plaque development through their interaction with endothelial and immune cells in the injured vessel wall. During the first steps of atherosclerosis, blood inflammatory leukocytes interact with the damaged endothelium in areas rich in platelet aggregates. In late stages of the disease, platelets secrete several inflammatory molecules, even without forming aggregates. These molecules exacerbate the inflammation and induce the transition from chronic to acute disease, featuring increased instability of the atherosclerotic lesion that results in plaque rupture and thrombosis. Moreover, platelets play an important role in vascular wall remodeling induced by chronic inflammation by controlling vascular cell differentiation and proliferation. In this review, we discuss the role of platelets as cell mediators that link inflammation and thrombosis in atherosclerotic disease and their potential in the development of new therapeutic tools to fight cardiovascular disease.

• Platelets, inflammation, atherosclerosis, cardiovascular disease

Acknowledgements

We are grateful to Simon Bartlett for English editing.

Declaration of interest: Work in the author's laboratories is supported by Centro de Estudios en Alimentos Procesados (CEAP), Conicyt-Regional, Gore Maule, R09I2001, Talca, Chile (Proyecto Basal); The Spanish Ministry of Science and Innovation (MICINN) and the European Regional Development Fund (grant SAF2010-16044); Instituto de Salud Carlos III (ISCIII) (Red de Enfermedades Cardiovasculares [RECAVA], grant RD06/0014/0021). O.M.P. holds a Juan de la Cierva contract (MICINN). The CNIC is supported by the MICINN and the Pro-CNIC Foundation. The authors report no declarations of interest.