TY - JOUR
T1 - Apoptosis as a therapeutic target in acutely ischemic myocardium
AU - Garg, Shaila
AU - Hofstra, Leo
AU - Reutelingsperger, Chris
AU - Narula, Jagat
PY - 2003/9
Y1 - 2003/9
N2 - In addition to necrosis, apoptosis makes a significant contribution to cell death following acute myocardial ischemia; apoptosis is particularly enhanced during repedusion. 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.
AB - In addition to necrosis, apoptosis makes a significant contribution to cell death following acute myocardial ischemia; apoptosis is particularly enhanced during repedusion. 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.
KW - Apoptosis
KW - Ischemia
UR - http://www.scopus.com/inward/record.url?scp=0141788070&partnerID=8YFLogxK
U2 - 10.1097/00001573-200309000-00009
DO - 10.1097/00001573-200309000-00009
M3 - Review article
C2 - 12960470
AN - SCOPUS:0141788070
SN - 0268-4705
VL - 18
SP - 372
EP - 377
JO - Current Opinion in Cardiology
JF - Current Opinion in Cardiology
IS - 5
ER -