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Oxygen free radical signaling in ischemic preconditioning
D K Das1, R M Engelman, N Maulik
1University of Connecticut School of Medicine, Farmington, USA.
Annals of the New York Academy of Sciences
|July 23, 1999
Summary
Reactive oxygen species act as crucial signaling molecules in preconditioning, mediating myocardial adaptation to ischemia. This review highlights tyrosine kinase and MAP kinases as key targets, linking preconditioning to gene expression via p38 MAP kinase and NF-kappa B.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Cell Signaling
Background:
- Preconditioning protects the heart against ischemic injury.
- Reactive oxygen species (ROS) are implicated as signaling molecules in this protective process.
- The precise molecular targets of ROS in preconditioning remain incompletely understood.
Purpose of the Study:
- To review the role of free radical signaling in preconditioning.
- To identify the molecular targets of ROS during myocardial adaptation to ischemia.
- To elucidate the signaling pathway linking preconditioning to gene expression.
Main Methods:
- Review of existing laboratory data and published studies.
- Analysis of the role of reactive oxygen species (ROS) as second messengers.
- Investigation of signaling pathways involving tyrosine kinase, MAP kinases, and NF-kappa B.
Main Results:
- Reactive oxygen species (ROS) function as second messengers in myocardial adaptation to ischemia.
- Tyrosine kinase and MAP kinases are identified as direct targets of ROS in the preconditioned myocardium.
- p38 MAP kinase activation is upstream of NF-kappa B, suggesting a role in gene expression regulation.
Conclusions:
- Free radical signaling is a critical mechanism in preconditioning.
- The p38 MAP kinase/NF-kappa B pathway is a key mediator linking preconditioning to the induction of stress-inducible genes.
- MAPKAP kinase 2 is likely the crucial link between preconditioning and adaptive gene expression.