Inflammatory role of platelets in acute coronary syndromes.

Content Provider	Semantic Scholar
Author	Aukrust, Pål Waehre, Torgun Damås, Jan Kristian Gullestad, Lars Solum, Nils Olav
Copyright Year	2001
Abstract	Increasing evidence shows that inflammatory mediators play a pathogenic role in atherogenesis and acute coronary syndrome. In particular, several reports suggest that inflammatory cytokines such as tumour necrosis factor á (TNFá), interleukin (IL)-1 and various chemokines (for example, IL-8) may enhance degradation of the connective tissue matrix protein by activating matrix metalloproteinases (MMPs) and induce apoptosis of cells within the atherosclerotic lesion, promoting plaque destabilisation and rupture. 2 These findings indicate a pathogenic link between persistent immune activation and plaque rupture in coronary artery disease. It is well established that platelets also contribute to the pathogenesis of acute coronary syndromes by promoting thrombus formation. However, recent studies suggest that these cells also may trigger an acute coronary event through other mechanisms, such as stimulation of an inflammatory response within the atherosclerotic plaque.
Starting Page	1133
Ending Page	1133
Page Count	1
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://heart.bmj.com/content/heartjnl/86/6/605.full.pdf
PubMed reference number	11711447v1
Volume Number	86
Issue Number	6
Journal	Heart
Language	English
Access Restriction	Open
Subject Keyword	Acute Coronary Syndrome Apoptosis Arteriopathic disease Atherogenesis Blood Platelets Connective Tissue Coronary Artery Disease Dental Plaque Interleukins Matrix Metalloproteinases Metalloproteases Neoplasms Promotion (action) Rupture Senile Plaques Thrombosis Tumor Necrosis Factors chemokine
Content Type	Text
Resource Type	Article