Journal
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
Volume 292, Issue 6, Pages F1673-F1680Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.00356.2006
Keywords
kidney; nitric oxide; cell death; cytoskeleton derangement
Categories
Ask authors/readers for more resources
During renal ischemia-reperfusion (I/R) injury, apoptosis has been reported as a very important contributor to final kidney damage. The determinant role of cytoskeleton derangement in the development of apoptosis has been previously reported, but a clear description of the different mechanisms involved in this process has not been yet provided. The aim of our study was to know the role of peroxynitrite as an inductor of cytoskeleton derangement and apoptosis during renal I/R. Based on a rat kidney I/R model, using experiments in which both the actin cytoskeleton and peroxynitrite generation were pharmacologically manipulated, results indicate that the peroxynitrite produced during the I/R-derived oxidative stress state is able to provoke cytoskeleton derangement and apoptosis development. Thus control of peroxynitrite generation during I/R could be an effective tool for the improvement of cytoskeleton damage and reduction of apoptosis incidence in renal I/R injury.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available