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Vessel wall--where coagulation meets cell biology and immunology.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Guzik, Tomasz J. Dulak, Józef |
| Copyright Year | 2012 |
| Abstract | Vascular inflammation, endothelial cell dysfunction and thrombosis are the most important mechanisms for cardiovascular diseases, which constitute major cause of morbidity and mortality (1, 2). These processes, often occurring in distinct vascular beds cause diverse symptoms of vascular pathology. For example, vascular dysfunction of the vessels in the heart manifests as coronary artery disease, while dysfunction of vessels in central nervous system lead to stroke but may also contribute to Parkinson’s disease or dementia. Renal vasculature dysfunction underlies renal insufficiency but also seems to be critical in hypertension. Therefore, vascular pathology remains the common denominator of numerous disease states. Molecular studies of the vessel wall have identified novel drug targets, while translational medicine provides clinical context to these findings. Most of new therapies target vascular inflammation, hypercoagulability and endothelial cell dysfunction. It becomes critical to better understand how these mechanisms interact in the vessel wall. In the current Theme Issue of Thrombosis and Haemostasis, stemming in part from the 6th European Meeting for Vascular Biology and Medicine, held in Krakow, Poland between 21 and 24 September, 2011 (http://emvbm2011.org), numerous aspects of vascular biology are discussed in the context of better identification of molecular mechanisms of atherothrombosis and future clinical usefulness of these findings ( Fig. 1). Fibrinogen and high sensitivity C-reactive protein (hsCRP) are the most important markers, which have been used to clinically link inflammation and thrombosis with cardiovascular risk. These molecules, however, may directly lead to vascular dysfunction and activate coagulation. The central role of fibrinogen as the precursor to fibrin, its ability to cross-link platelets, and its effects on blood viscosity, suggest that fibrinogen is the major risk factor for cardiovascular disease and thrombotic events (3). Fibrinogen, which is produced in the hepatocytes, is also an important acute phase protein, associated with systemic inflammation. Interleukin 6 (IL-6) response element is the critical factor in the regulation of fibrinogen gene expression, which further links thrombosis to inflammation (3). These aspects of the biology and genetics of the regulation of fibrinogen gene expression are comprehensively reviewed by Fish et al. (3). Fibrinogen level in plasma of patients is influenced by environmental and genetic components, with the latter contributing 20 to 50% of the variability (3). Thus, understanding the genetic mechanisms of this variability is critical for future use of fibrinogen as a marker for cardiovascular risk. The three fibrinogen genes, FGA, FGB and FGG, are coordinately expressed in hepatocytes from a compact gene cluster. In the original contribution published in this issue of |
| File Format | PDF HTM / HTML |
| DOI | 10.1160/TH12-08-0558 |
| PubMed reference number | 22898929 |
| Journal | Medline |
| Volume Number | 108 |
| Issue Number | 3 |
| Alternate Webpage(s) | https://th.schattauer.de/contents/archive/issue/1575/manuscript/18050/download.html |
| Alternate Webpage(s) | https://th.schattauer.de/en/contents/archive/issue/1575/manuscript/18050/download.html |
| Alternate Webpage(s) | https://doi.org/10.1160/TH12-08-0558 |
| Journal | Thrombosis and haemostasis |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
