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Endothelial dysfunction, impaired endogenous platelet inhibition and platelet activation in diabetes and atherosclerosis.

Abstract：

:Platelet activation induces rapid thrombus formation at a ruptured atherosclerotic plaque leading to acute vessel occlusion and a fatal or non-fatal cardiovascular event. More recent evidence suggests that activated platelets play an additional central role during the initiation of atherosclerosis, essentially facilitating leukocyte adhesion and recruitment. Endothelial dysfunction is a common and early feature of cardiovascular diseases characterized by reduced bioavailability of prostacyclin and nitric oxide (NO). Subsequently impaired endogenous platelet inhibition causes platelet activation in pre-atherosclerotic vascular disease resulting in enhanced platelet susceptibility to agonists released from the inflamed endothelium. Platelet adhesion to inflammatory, dysfunctional endothelium precedes leukocyte adhesion. Indeed, adherent activated platelets are mandatory for leukocyte recruitment in the early phases of atherosclerosis under arterial flow conditions. Increased expression of chemokines in atherosclerotic plaques and the inflamed endothelium initiates and facilitates pro-inflammatory processes in leukocytes and the vascular wall. Apart from their chemotactic properties, some chemokines such as fractalkine contribute to platelet activation. Moreover, fractalkine induces leukocyte recruitment to inflamed endothelial cells under arterial flow by activating adherent platelets. An aggressive form of atherosclerosis is found in patients with diabetes. Since diabetes is currently considered as a risk equivalent for coronary artery disease, the interaction between oxidative stress, endothelial dysfunction, impaired endogenous platelet inhibition and platelet activation is discussed in the light of diabetes. Defective regulation of platelet activation/aggregation is a predominant cause for arterial thrombosis, the major complication of atherosclerosis triggering myocardial infarction and stroke.

journal_name

Curr Vasc Pharmacol

journal_title

Current vascular pharmacology

authors

Schäfer A,Bauersachs J

doi

10.2174/157016108783331295

subject

Has Abstract

pub_date

2008-01-01 00:00:00

pages

52-60

issue

eissn

1570-1611

issn

1875-6212

journal_volume

pub_type

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Endothelial dysfunction, impaired endogenous platelet inhibition and platelet activation in diabetes and atherosclerosis.