The cell cycle and cardiovascular diseases.
Cardiovascular diseases are the leading cause of morbidity and mortality in industrialized countries. Most cardiovascular diseases result from complications of atherosclerosis, which is a chronic and progression inflammatory condition characterized by excessive cellular proliferation of vascular smooth muscle cells, endothelial cells and inflammatory cells leading to occlusive vascular disease, myocardial infarction and stroke. Recent studies have revealed the important role of the cyclins, the cyclin-dependent kinases (CDKs), and the cyclin-dependent kinase inhibitors (CKIs) in vascular and cardiac tissue injury, inflammation and wound repair. Tissue remodeling in the cardiovascular system is a regulated balance between pro- and anti-proliferative molecules, and this balance becomes derailed in cardiovascular pathology. Understanding the circuitry of the cyclin-CDK-CKI interactions in normal physiology and disease pathology allows a better understanding of the molecular mechanisms of cardiovascular diseases and permits the rationale design of new classes of therapeutic agents for these diseases.
Cardiovascular Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.
Manfred
M
Boehm
Elizabeth G
EG
Nabel
D000818:Animals; D002318:Cardiovascular Diseases / Q000201:enzymology* / Q000235:genetics; D002453:Cell Cycle / Q000235:genetics*; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000201:enzymology* / Q000235:genetics; D018844:Cyclin-Dependent Kinases / Q000235:genetics / Q000378:metabolism; D016213:Cyclins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D006965:Hyperplasia / Q000201:enzymology / Q000235:genetics
D018797:Cell Cycle Proteins; D016213:Cyclins; D018844:Cyclin-Dependent Kinases