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2023, Number 2

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Sal Jal 2023; 10 (2)

D-dimer and adhesion molecules related to thromboembolic disease

Guzmán-Silahua S, Barreno-Rocha SG, Rodríguez-Dávila SC, Sánchez-Cazares K, Barreno-Rocha MA, Rubio-Jurado B, Nava-Zavala AH

Language: Spanish
References: 49
Page: 81-90
PDF size: 270.95 Kb.


ABSTRACT

Thromboembolic disease (TE) and inflammation are physiologically linked processes. TE is one of the main causes of morbidity and mortality and the understanding of vascular inflammation, platelet adhesion and atherothrombosis has led to the knowledge of molecular mechanisms of cellular interaction mediated by adhesion molecules, which facilitate the rolling, adhesion and migration of leukocytes and platelets to sites of inflamed endothelium, facilitating basic functions of the immune system in order to eliminate pathogens and thrombus formation. Cell adhesion molecules (CAM) are receptors that belong to the immunoglobulin superfamily, mediate cell interaction by adhesion to other cells and the extracellular matrix, regulate leukocyte migration, and have been detected at sites of atherothrombosis. Leukocytes and endothelial cells express adhesion molecules under the influence of IL-1, TNF-α, and interferon-γ. Selectins are surface molecules that participate in cell adhesion and are involved in processes such as diapedesis, thrombosis, acute and chronic inflammation, and ischemia-reperfusion injury. Integrins are integral proteins, such as the major platelet receptor, integrin αIIbβ3 serves to bind collagen, fibrinogen, von Willebrand factor, fibronectin, and thrombospondin. Activated platelets present at a site of damage provide a prothrombotic and procoagulant surface and can initiate an acute inflammatory response, mediated by P-selectin expression in the endothelium, which generates its activation by platelet secretion of IL-1β, the activated endothelial cell promotes chemotaxis, adhesion, migration, proteolysis and thrombosis.


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