The role of Akt (protein kinase B) and protein kinase C in ischemia-reperfusion injury.

Abstract

Stroke is a leading cause of long-term disability and death in the United States. Currently, tissue plasminogen activator (tPA), is the only Food and Drug Administration-approved treatment for acute ischemic stroke. However, the use of tPA is restricted to a small subset of acute stroke patients due to its limited 3-h therapeutic time window. Given the limited therapeutic options at present and the multi-factorial progression of ischemic stroke, emphasis has been placed on the discovery and use of combination therapies aimed at various molecular targets contributing to ischemic cell death. Protein kinase C (PKC) and Akt (protein kinase B) are serine/threonine kinases that play a critical role in mediating ischemic-reperfusion injury and cellular growth and survival, respectively. The present review will examine the role of PKC and Akt in the cellular response to ischemic-reperfusion injury.

• Authors: Ethan Y Zhao, Aslan Efendizade, Lipeng Cai, Yuchuan Ding
• Journal: Neurological research (Neurol Res) Vol. 38 Issue 4 Pg. 301-8 (Apr 2016) ISSN: 1743-1328 [Electronic] England
• PMID: 27092987 (Publication Type: Journal Article, Review)

Chemical References

• Proto-Oncogene Proteins c-akt
• Protein Kinase C

Topics

• Animals
• Brain Ischemia (drug therapy, enzymology)
• Humans
• Models, Biological
• Protein Kinase C (metabolism)
• Proto-Oncogene Proteins c-akt (metabolism)
• Reperfusion Injury (drug therapy, enzymology)