Apoptosis as a therapeutic target in acutely ischemic myocardium.
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.
Garg
Shaila
S
Drexel University College of Medicine, Philadelphia, Pennsylvania, USA. shaliagarg@yahoo.com
Hofstra
Leo
L
Reutelingsperger
Chris
C
Narula
Jagat
J
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
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors