title: Apoptosis as a therapeutic target in acutely ischemic myocardium.
abstract: In addition to necrosis, apoptosis makes a significant contribution to cell death following acute myocardial ischemia; apoptosis is particularly enhanced during reperfusion. Several studies are beginning to indicate that the cell death by apoptosis may be preventable. A boost in the research in this direction has been provided by noninvasive means of detection of apoptosis, such as that achieved by technetium-99m labeled Annexin-A5 scintigraphy. Various levels within the apoptotic cascade are being investigated as therapeutic targets. Caspase inhibitors, mitochondrial stabilizers, and Na+-H+ exchanger inhibitors reduce cell death by apoptosis and infarct size. Although most of the evidence at present is limited to the laboratory animals, this approach seems to hold a promise for the future.
authors.affiliation: Drexel University College of Medicine, Philadelphia, Pennsylvania, USA. shaliagarg@yahoo.com
authors.forename: Shaila
authors.initials: S
authors.lastname: Garg
authors.forename: Leo
authors.initials: L
authors.lastname: Hofstra
authors.forename: Chris
authors.initials: C
authors.lastname: Reutelingsperger
authors.forename: Jagat
authors.initials: J
authors.lastname: Narula
mesh_terms: D000208:Acute Disease; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D015316:Genetic Therapy; D006801:Humans; D017202:Myocardial Ischemia / Q000503:physiopathology* / Q000517:prevention & control*; D015425:Myocardial Reperfusion; D011877:Radionuclide Imaging
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors