Advances in research on the effects of platelet activation in acute lung injury (Review)

Abstract

Acute lung injury (ALI) is an acute hypoxic respiratory insufficiency or failure caused by various factors inside and outside the lungs. ALI is associated with high morbidity and a poor prognosis in hospitalized patients. The lungs serve as a reservoir for platelet precursor megakaryocytes and are closely associated with platelets. Platelets not only play a central role in hemostasis, coagulation and wound healing, but can also act as inflammatory cells capable of stimulating non-hemostatic immune functions under inflammatory conditions, participating in the progression of various inflammatory diseases, and can result in tissue damage. Therefore, it was speculated that platelets may play an important role in the pathogenesis of ALI. In this review, the latest research progress on secretion of bioactive mediators from platelets, platelet activation-related signaling pathways, and the direct contact reactions between platelets and neutrophils with endothelial cells that result in ALI are described, providing evidence to support the importance of the consideration of platelets in the search for ALI interventional targets.

Keywords: acute lung injury; inflammation; mechanism of injury; platelets.

Figure 1

Secretory reactive substances released from platelets that modulate lung injury. VEGF, vascular endothelial growth factor; PMP, platelet-microparticle; TXA2, thromboxane A2; COX-2, cyclooxygenase 2; ICAM-1, intercellular adhesion molecule-1.

Figure 2

Platelet receptor ligand signaling pathway activation regulates lung injury. ITAM, immunoreceptor tyrosine-based activation motif; CLEC-2, C-type lectin-like receptor 2; MAPK1, mitogen-activated protein kinase 1; GPCR, G protein-coupled receptor; ADP, adenosine diphosphate; PKC, protein kinase C; Syk, spleen tyrosine kinase.

Figure 3

Through direct contact with cells, Platelets modulate lung injury. NETs, neutrophil extracellular traps; PRR, pattern recognition receptor; RANTES, regulated upon activation, normal T cell expressed and secreted factor.