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Follow on Google News | Why kidney disease damages the vascular systemBy: Austrian Science Fund FWF Patients suffering from chronic renal disease frequently die from cardiovascular complications. A damaged and poorly functioning vascular system is the reason for such complications. A team working with Gunther Marsche at the Medical University of Graz on a project supported by the FWF investigated the extent to which a specific decomposition product (cyanate) of urea, which occurs in a concentrated form in the blood of patients with renal disease, is responsible. One team – two discoveries "We were able to identify two previously unknown mechanisms in human tissue and in an animal model by which cyanate can lead to a dysfunctional vascular system in patients with chronic renal disease", explains Gunther Marsche. "In the first mechanism, cyanate causes an adverse change in a lipoprotein, which, in its unchanged state, is key to the healthy functioning of blood vessels. In the second case, cyanate activates a gene that can amplify inflammatory responses in the vascular system." From good to bad cholesterol The lipoprotein that is modified by cyanate is the High Density Lipoprotein (HDL), also known as "good" cholesterol. As the team working with Marsche was able to demonstrate, HDL undergoes a chemical change known as carbamylation. The results are drastic, as Marsche outlines: "While, prior to this modification, HDL helped to prevent vascular constriction, this protective effect is dramatically reduced by carbamylation. In extreme cases, it can even be a factor in vascular constriction." Gene activation The second effect that cyanate has on the vascular system and which was identified by Marsche's group, is caused by the activation of a gene. This codes for a so-called adhesion molecule, which is located on the cell membrane of the endothelial cells, i.e. on the cell layer that lines a vessel. The protein known as ICAM-1 functions by pointing certain blood cells (leucocytes) From knowledge to treatment The findings from this FWF project are urgently needed, as the average age of the general population increases and with it the number of patients with chronic renal disease. Their mortality increases sharply in particular as a result of secondary cardiovascular disease. To date, however, little is known about how these sequelae occur. For Marsche, the fundamental importance of these discoveries within the framework of the FWF project is therefore clear: "The data from this FWF project provides an approach for the clinical evaluation of substances that counteract cyanate in the blood. This could lead to the development of medications and treatments that would facilitate a much better quality of life for patients with renal disease." Image and text available from Monday, 8 June 2015, from 10.00 am CEST at: http://www.fwf.ac.at/ Personal details Gunther Marsche works in the Institute of Experimental and Clinical Pharmacology (http://www.medunigraz.at/ Scientific Contact: Prof. Gunther Marsche Medical University of Graz Institute of Experimental and Clinical Pharmacology Universitätsplatz 4 8010 Graz, Austria T +43 / 316 / 380 - 4513 E gunther.marsche@ W http://www.medunigraz.at Austrian Science Fund FWF: Marc Seumenicht Haus der Forschung Sensengasse 1 1090 Vienna, Austria T +43 / 1 / 505 67 40 - 8111 E marc.seumenicht@ W http://www.fwf.ac.at Copy Editing & Distribution: PR&D – Public Relations for Research & Education Mariannengasse 8 1090 Vienna, Austria T +43 / 1 / 505 70 44 E contact@prd.at W http://www.prd.at End
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