Platelet Function and Coronary Microvascular Dysfunction
(2020) Microcirculation: From bench to bedsite — ISBN: [978-3-030-28199-1], 63-76, published
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- Abstract
- The ability of platelets to activate and aggregate to form blood clots in response to endothelial injury is well established. They are therefore critical contributors to ischaemia in atherothrombosis [1]. However, their role in cardiovascular disease is not limited to end-stage thrombosis in large vessels [2]. Abundant experimental evidence has established that activated platelets are also important mediators of microvascular thrombosis and promote the inflammatory response during ischaemia-reperfusion (IR) injury [3–5]. While platelets do not physically interact with the healthy endothelium, they can bind to the wall of hypoxic microvessels and release a plethora of inflammatory mediators that further enhance the activation of the endothelial monolayer and the recruitment of circulating leukocytes (monocytes, neutrophils, T-cells) [2]. In addition, deposition of platelets to the dysfunctional endothelium can lead to vasoconstriction which accelerates microvascular occlusion, thereby impairing tissue perfusion [3]. In this chapter, we discuss the role of platelets in promoting microvascular dysfunction and inflammation during IR injury. Focus is placed on the cross-talk between platelets and other cell types (endothelial cells [ECs] and leukocytes) via platelet adhesion receptors and platelet-derived proinflammatory mediators. We also consider new paradoxical functionalities of platelets promoting cardiac recovery after myocardial infarction (MI).
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Citations
Horman, S., Dechamps, M., Octave, M., Lepropre, S., Bertrand, L., & Beauloye, C. (2020). Platelet Function and Coronary Microvascular Dysfunction. In Dorobantu Maria, Badimon Lina (ed.), Microcirculation: From bench to bedsite (pp. 63-76). Springer Nature. https://doi.org/10.1007/978-3-030-28199-1_5