Journal
EXPERT OPINION ON THERAPEUTIC TARGETS
Volume 9, Issue 3, Pages 447-456Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1517/14728222.9.3.447
Keywords
apoptosis; cardiac hypertrophy; cardioprotection; glycogen synthase kinase (GSK); heart; metabolism
Categories
Funding
- NHLBI NIH HHS [R01 HL039752] Funding Source: Medline
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Cardiovascular disease is the major cause of morbidity and mortality in western countries such as the US. Myocardial infarction leads to loss of myocytes and with extremely limited ability to replenish cardiomyocytes, the heart exhibits depressed contractility. This ultimately results in hypertrophy of the remaining viable myocytes, which is the primary predictor for heart failure. Thus, drug therapies which can reduce myocyte cell death and reduce postischaemic dysfunction would be expected to greatly reduce cardiac hypertrophy and subsequent heart failure and death. Inhibition of glycogen synthase kinase (GSK)-3 beta has been proposed as a strategy to improve postischaemic cardiomyocyte survival, as inhibition of GSK-3 beta has been shown to reduce myocardial cell death following ischaemia and reperfusion. Therapies for inhibiting GSK are feasible as there are a number of newly developed specific inhibitors of GSK available, although most of these drugs have not been tested in long-term animal studies.
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