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Review
. 2014 Aug;19(8):1230-5.
doi: 10.1016/j.drudis.2014.04.001. Epub 2014 Apr 18.

Thrombosis, platelets, microparticles and PAH: more than a clot

Katie L Lannan  1 , Richard P Phipps  2 , R James White  3
Affiliations
Review

Thrombosis, platelets, microparticles and PAH: more than a clot

Katie L Lannan et al. Drug Discov Today. 2014 Aug.

Abstract

Pulmonary arterial hypertension (PAH) is a progressive disease that involves pathological remodeling, vasoconstriction and thrombosis. Alterations in hemostasis, coagulation and platelet activation are consistently observed in PAH patients. Microparticles derived from platelets, inflammatory cells and the endothelium are an increasingly well-recognized signal in a variety of cardiovascular diseases, including PAH. This review will focus on the roles of coagulation, thrombosis, platelet activation and microparticles in the pathology and progression of PAH.

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Conflict of interest statement

Conflict of Interest

The authors have no conflict of interest to declare.

Figures

Figure 1
Figure 1. Potential role of platelets in the development and progression of PAH
Endothelial dysfunction and altered hemostasis leads to an imbalance of inhibitors and activators of platelets. Activated platelets release proinflammatory and prothrombotic mediators and generate highly bioactive platelet microparticles. Activated platelets adhere to endothelial cells via CD62P and its ligand, PSGL1. Large amounts of sCD40L are released from platelets. which induces proinflammatory mediator release, leading to immune cell recruitment. Soluble CD40L further induces smooth muscle cell (SMC) proliferation and hypertrophy. Platelets and platelet microparticles bind to and activate immune cells.
See this image and copyright information in PMC

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