Clinical implications of apoptosis in ischemic myocardium

Tiziano M. Scarabelli, Richard Knight, Anastasis Stephanou, Paul Townsend, Carol Chen-Scarabelli, Kevin Lawrence, Roberta Gottlieb, David Latchman, Jagat Narula

Research output: Contribution to journalArticlepeer-review

71 Scopus citations


Apoptosis, a genetically programmed form of cell death, contributes to myocyte cell loss in a variety of cardiac pathologies, including cardiac failure and those related to ischemia/reperfusion injury. The apoptotic program is complex, involving both pro- and anti-apoptotic proteins, and apoptosis occurs when the equilibrium between these opposing factors is perturbed. Some of these factors are intrinsic to the apoptotic pathway, such as the pro- and anti-apoptotic members of the Bcl2 family. Other, extrinsic, cellular factors can also modify the outcome of the response to an apoptotic stimulus. In this review, we have focused on some of these extrinsic factors, such as STAT-1 as a pro-apoptotic agent and the urocortins and Bag-1 as anti-apoptotic factors, since these may be potential therapeutic targets. In addition, we discuss the profound cytoprotective effects of the antibiotic, minocycline.

Original languageEnglish
Pages (from-to)181-264
Number of pages84
JournalCurrent Problems in Cardiology
Issue number3
StatePublished - Mar 2006


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