In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

We use cookies to optimise the design of this website and make continuous improvement. By continuing your visit, you consent to the use of cookies. Learn more

Inflammatory mechanisms in atherosclerosis - genetics - Title: Inflammatory mechanisms in atherosclerosis - genetics

Genomics


Dr. Daemen presented the important role of genomics of foam cell macrophages in atherosclerosis. He states that an important element is hypoxia and that specific genes (n=42) are expressed in macrophages in stable advanced atheromatous plaque. Increased TWST1 expression levels occur in oxLDL stimulated macrophages.

Prof. Newby presented the role of proteomics and proteases in foam cells. Especially he states that MMP-12 marks foam cells only in advanced plaques. He stated also that there are differences in the secretion of MMP in the early and late macrophages.

Dr. Kovanen presented the role of mast cells. He showed that mast cells are found in totally occluded human coronary arteries and in culprit coronary arteries, which leads to acute myocardial infarction. Factors which activate mast cells are oxidative stress and other inflammatory markers. They release proteases, especially lipid proteases, and inflammatory mediators.

Dr. Back presented the role of leukotrienes in atherosclerosis. He said that inhibition of leukotrienes leads to reduced intima-media thickness. Also he presented data indicating that they interact with leukocytes, endothelial cells, and vascular smooth muscle cells. Inhibition of leukotrienes may be a new target for treatment in atherosclerosis.

Dr. Pasterkamp presented local inflammatory markers. He showed that a strong predictor in carotid plaque for future events is the presence of thrombus. He also stated that osteopontin is related to the future cardiovascular event (myocardial infarction, thrombosis, peripheral artery disease). The predictive value of plaque osteopontin is not related to CD48 and other inflammatory markers.

Conclusion:

In conclusion, new data suggest the important role of genomics and proteonomics in the regulation of foam cells and mast cells, which play a crucial role in plaque stability and atherosclerosis.

References


948000

SessionTitle:

Inflammatory mechanisms in atherosclerosis Symposium - State of the Art in Basic Science

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.