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EN
The participation of lipid peroxidation in pathogenesis of atherosclerosis is described. The role of antioxidants as well as the importance of dysfunction of endothelium cells in the vessel wall injury is shown.
Biotechnologia
|
2000
|
issue 1
135-146
EN
Gene therapy is suggested to be beneficial for the treatment of diseases which are difficult or impossible to be cured by classical pharmacotherapy. Thus, the transfer of genetic material of potential therapeutic properties may be particularly helpful in the treatment of hereditary genetic disorders and cancer. However, serious technical obstacles, especially the lack of efficient vectors for the delivery of therapeutic genes have so far prevented the achievement of convincing therapeutic effects. On the other hand, the complications of atherosclerosis, such as heart or peripheral ischaemia, seem to be good candidates for genetic strategies aimed particularly at stimulation of angiogenesis. As in this case therapeutic genes should be expressed locally and in a short time there is a good chance that the application of this therapy will take place earlier than in the case of other disorders. In this paper the first gene therapy clinical trials in human cardiovascular diseases are described. The latest investigations on the basic mechanisms of the blood vessel wall physiology and relationships between factors involved in angiogenesis are also briefly mentioned.
EN
Work presents current views on involvment of free radicals in inhibition of development of artriosclerosis by calcium (ACa).The importance of other substances, which interferes with calcium ions can contribute to the inhibiton of arteriosclerosis development.
EN
Heparin is a highly sulfated glycosaminoglycan with many functions such as antilipemic and antithrombotic.In spite os these activities heparin is able to inhibit vacsular smooth muscle cells proliferation and mmigration what seems to be very important event in the pathogenesis of atherosclerosos.The molecular mechanism of the action of heparin on smooth muscle cells is not yet understood.Heparin inhibits growth factors binding to their receptors,oncogenes expressionand has influence on the extracellular matrix protein deposition in the artery wall.
EN
Myocardial infarction and stroke are the major cause of death in developed countries and are the clinical manifestation of atherosclerosis and hypertension. Both the environmental factors and genetic predisposition have an influence on the pathogenesis of these diseases. Despite we know lots of environmental risk factors and we made important advances in the prevention and treatment of mentioned diseases, our knowledge about the pathogenic linkage between genetic predisposition and cardiovascular diseases is still very little. Activation of the renin-angiotensin system has been proposed as a very important step in the pathogenesis of hypertension and atherosclerosis. In spite of vasoconstrictor activity, angiotensin II can stimulate migration and proliferation of vascular smooth muscle cells, macrophage-foam cells formation, adhesion and agregation of platelets and fibrinolytic system inhibition. Angiotensin convertin enzyme inhibitors reduce the development of the atherosclerotic process after vascular injury and in hyperlipidemic animals. Blockade of renin-angiotensin system seems to be also effective in secondary prevention of myocardial infarction in men. In sum, the genetic variations inside the renin-angiotensin system which may affect the function of its components might have an influence on genetic predisposition to cardiovascular diseases. The paper deals with the current state of knowledge on association between polymorphic variations in renin gene, angiotensinogen gene, angiotensin converting enzyme gene and AT1 receptor gene and primary hypertension, ischeamic heart disease and myocardial infarction.
EN
The activation of the renin-angiotensin system has been proposed as a very important step in the pathogenesis of atherosclerosis. Accordingly, ACE-inhibitors and angiotensin II receptors antagonists showed their ability to reduce the atherosclerotic process in animals. Inhibition of renin-angiotensin system reduces the development of atherosclerotic lesion either in cholesterol-fed animals and in animals after vascular injury. The precise mechanism for this action may depend on the inhibition of other than hypertensive property of angiotensin II.
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