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Reeve, JLV,Duffy, AM,O'Brien, T,Samali, A
2005
July
Don't lose heart - therapeutic value of apoptosis prevention in the treatment of cardiovascular disease
Published
1
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cardiovascular disease apoptosis ischemia/reperfusion (I/R) mitochondria anti-apoptosis therapy NECROSIS-FACTOR-ALPHA ADENINE-NUCLEOTIDE TRANSLOCATOR PERMEABILITY TRANSITION PORE ENDOPLASMIC-RETICULUM STRESS ISCHEMIA-REPERFUSION INJURY ACUTE MYOCARDIAL-INFARCTION CASPASE RECRUITMENT DOMAIN CARDIAC MYOCYTE APOPTOSIS FAS-MEDIATED APOPTOSIS CELL-DEATH PROTEASES
Cardiovascular disease is a leading cause of death worldwide. Loss of function or death of cardiomyocytes is a major contributing factor to these diseases. Cell death in conditions such as heart failure and myocardial infarction is associated with apoptosis. Apoptotic pathways have been well studied in non-myocytes and it is thought that similar pathways exist in cardiomyocytes. These pathways include death initiated by ligation of membrane-bound death receptors, release of pro-apoptotic factors from mitochondria or stress at the endoplasmic reticulum. The key regulators of apoptosis include inhibitors of caspases (IAPs), the Bcl-2 family of proteins, growth factors, stress proteins, calcium and oxidants. The highly organized and predictive nature of apoptotic signaling means it is amenable to manipulation. A thorough understanding of the apoptotic process would facilitate intervention at the most suitable points, alleviating myocardium decline and dysfunction. This review summarizes the mechanisms underlying apoptosis and the mediators/regulators involved in these signaling pathways. We also discuss how the potential therapeutic value of these molecules could be harnessed.
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