Linked Life Data

9415290

Source:http://linkedlifedata.com/resource/pubmed/id/9415290

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1998-1-27
pubmed:abstractText
Conventional antithrombotic treatments with antiplatelet, anticoagulant or fibrinolytic drugs are not uniformly successful and are associated with hemorrhagic side effects. Thus, new approaches to the prevention and treatment of arterial thrombosis are desirable. The gene transfer approach is particularly attractive because of its unique ability to express an antithrombotic gene at selected sites of the vessel wall (where thrombosis is threatened) while avoiding systemic anticoagulation. Clinical conditions potentially amenable to antithrombotic gene therapy include coronary artery bypass grafting, percutaneous transluminal coronary angioplasty, peripheral artery angioplasty or thrombectomy, intravascular stenting, and vascular graft prostheses. Gene therapy may prove effective in preventing subacute thrombosis in these settings and, eventually, may play an adjuvant role to systemic thrombolysis in the treatment of acute arterial occlusion. The introduction of an antithrombotic gene into the arterial wall can be achieved either by direct in vivo gene transfer (e.g., by luminal administration of a viral vector) or by in vitro genetic manipulation of cells before their seeding onto vascular grafts, stents, or denuded arteries. The direct gene transfer approach has been used to deliver antithrombotic genes to animal arteries in vivo. Antithrombotic genes used to date include those encoding enzymes of the prostacyclin synthetic pathway, nitric oxide synthase, the thrombin inhibitor hirudin, and thrombomodulin. The in vitro gene transfer approach has been used to enhance the fibrinolytic activity of vascular grafts by overexpressing plasminogen activators. If the initial successes of gene therapy for thrombotic disease in animal models are confirmed by longer-term experiments, and if new vectors are developed which permit prolonged transgene expression without inflammation, human studies can be initiated.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0008-6363
pubmed:author
pubmed:issnType
Print
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
459-69
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Gene therapy for arterial thrombosis.
pubmed:affiliation
Gladstone Institute of Cardiovascular Disease, Department of Medicine, University of California, San Francisco 94141-9100, USA.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't