Published online before print October 27, 2005, doi: 10.1161/01.STR.0000189996.71237.f7
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(Stroke. 2005;36:2781.)
© 2005 American Heart Association, Inc.
Progress Reviews |
The Role of Protein Kinase C in Cerebral Ischemic and Reperfusion Injury
From the Stanford University School of Medicine, California.
Correspondence to Daria Mochly-Rosen, Stanford University School of Medicine, CCSR, Room 3145A269 Campus Dr, Stanford, CA 94305-5174. E-mail mochly{at}stanford.edu
Background and Purpose— Stroke is a leading cause of disability and death in the United States, yet limited therapeutic options exist. The need for novel neuroprotective agents has spurred efforts to understand the intracellular signaling pathways that mediate cellular response to stroke. Protein kinase C (PKC) plays a central role in mediating ischemic and reperfusion damage in multiple tissues, including the brain. However, because of conflicting reports, it remains unclear whether PKC is involved in cell survival signaling, or mediates detrimental processes.
Summary of Review— This review will examine the role of PKC activity in stroke. In particular, we will focus on more recent insights into the PKC isozyme-specific responses in neuronal preconditioning and in ischemia and reperfusion-induced stress.
Conclusion— Examination of PKC isozyme activities during stroke demonstrates the clinical promise of PKC isozyme-specific modulators for the treatment of cerebral ischemia.
Key Words: cerebral infarction • cerebral ischemia • neuroprotection
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