Molecular mechanisms involved in atherosclerosis.
BACKGROUND
Research in atherosclerosis is a good example how helpful different disciplines such as clinicians, epidemiologists and basic science can collaborate. In recent years our knowledge on cellular and subcellular mechanisms involved in initiation and progress of atherosclerosis has expanded due to the shared knowledge of different disciplines and thanks to new technologies in molecular biology.
The understanding of the molecular basis of inborn errors of LDL metabolism - such as familial hypercholesterolemia due to a defect of the LDL receptor - provided us new insights in physiology and pathophysiology of LDL metabolism. Most recently we have learned much about the vasoprotective HDL cholesterol. HDL is the major player in reverse cholesterol transport and some of its receptors such as ABCA1 and SR-BI were identified. This knowledge gives us a deeper understanding of the complex system which performs reverse cholesterol transport from peripheral tissue and the vessel wall back to the liver.
Furthermore the process of formation and progression of the atherosclerotic plaque has been the focus of recent research. The stability or instability of plaques is depending on the complex interaction of adhesion molecules, monocytes, macrophages, endothelial cells, cytokines, transmitters and proteinases. Since we are unable to prevent plaque formation completely, the stabilization of plaques is a major goal for the coming years. Despite some success (such as the use of statines and ACE inhibitors) there is still a long way to go.
Soufi
Muhidien
M
Department of Internal Medicine, Philipps-University Marburg, Germany.
Sattler
Alexander M
AM
Maisch
Bernhard
B
Schaefer
Jürgen R
JR
D000293:Adolescent; D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics / Q000378:metabolism; D001161:Arteriosclerosis / Q000188:drug therapy / Q000209:etiology / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D001808:Blood Vessels / Q000378:metabolism; D002417:Cattle; D002478:Cells, Cultured; D002648:Child; D002784:Cholesterol / Q000378:metabolism; D008076:Cholesterol, HDL / Q000378:metabolism; D003327:Coronary Disease / Q000209:etiology; D016207:Cytokines / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D006579:Heterozygote; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications* / Q000188:drug therapy; D006938:Hyperlipoproteinemia Type II / Q000150:complications / Q000235:genetics; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008077:Lipoproteins, LDL / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008967:Molecular Biology; D009154:Mutation; D009203:Myocardial Infarction / Q000209:etiology; D011110:Polymorphism, Genetic; D011973:Receptors, LDL / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D012106:Research; D012307:Risk Factors; D013631:Tangier Disease / Q000235:genetics / Q000378:metabolism
D000806:Angiotensin-Converting Enzyme Inhibitors; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D016207:Cytokines; D000960:Hypolipidemic Agents; D008077:Lipoproteins, LDL; D011973:Receptors, LDL; D002784:Cholesterol