title: The molecular mechanisms of vascular restenosis: Which genes are crucial?
abstract: Many patients with coronary heart disease undergo percutaneous transluminal coronary angioplasty (PTCA) to improve myocardial tissue perfusion. However, a major complication after revascularisation procedures is restenosis of the injured artery. The molecular mechanism involved is not fully elucidated and no successful treatment is currently available. Animal models are preliminary tools that can help improve our understanding of the pathogenesis and treatment of restenosis in humans. Attracted by well-defined genetic systems, a number of investigators began to use the mouse as an experimental system for restenosis research. They demonstrated that several stages involved in this process include thrombus formation, inflammatory cell infiltration and smooth muscle cell (SMC) accumulation to form neointimal lesions. By using transgenic and knockout mice a number of genes related to these processes have been found to play a major role in mediating lesion formation, e.g. the plasminogen system, matrix metalloproteinases (MMP), adhesion molecules, cytokines and signal transducers. This review will not attempt to cover all aspects of related genes or molecules, but will rather focus on several groups of genes, by which the major progress in understanding the mechanisms of the disease has been made. The information obtained by using animal models could be essential for a better understanding of the pathogenesis of restenosis in humans and to provide a basis for therapeutic intervention.
authors.affiliation: Department of Cardiac and Vascular Sciences, St. George's University of London, London, UK.
authors.forename: Jemma
authors.initials: J
authors.lastname: Bhoday
authors.forename: Sampath
authors.initials: S
authors.lastname: de Silva
authors.forename: Qingbo
authors.initials: Q
authors.lastname: Xu
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000818:Animals; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D003327:Coronary Disease / Q000628:therapy*; D023903:Coronary Restenosis / Q000209:etiology / Q000235:genetics* / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation; D006133:Growth Substances / Q000235:genetics / Q000378:metabolism; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D045726:Metalloproteases / Q000235:genetics / Q000378:metabolism; D051379:Mice; D023421:Models, Animal; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics / Q000378:metabolism; D010960:Plasminogen Activators / Q000235:genetics / Q000378:metabolism
chemical_list: D015815:Cell Adhesion Molecules; D018925:Chemokines; D016207:Cytokines; D006133:Growth Substances; D047908:Intracellular Signaling Peptides and Proteins; D017395:Plasminogen Activator Inhibitor 1; D019001:Nitric Oxide Synthase; D045726:Metalloproteases; D010960:Plasminogen Activators