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JCI online early table of contents: April 6, 2009
Date:4/6/2009

as renal tubular cells is a major cause of acute kidney failure, which is increasing in prevalence. In particular, damage to the energy generating compartments of the cell, which are known as mitochondria, is central to renal tubular cell death. Zheng Dong and colleagues, at the Medical College of Georgia, Augusta, have now provided new insight into the mitochondrial changes that occur in acute rodent kidney injury, information that they hope might provide new avenues of research for those developing drugs to combat this condition.

In the study, analysis of rat renal tubular cells in vitro following exposure to conditions that induce acute kidney injury in vivo, revealed that mitochondria fragmented before the cells died. Furthermore, both knocking down expression of the protein Drp1, which is known to be involved in mitochondrial fission, and blocking its function substantially reduced mitochondrial fragmentation and apoptotic cell death. Consistent with these data, mitochondrial fragmentation was observed in two mouse models of acute kidney injury and treatment with a newly identified pharmacological inhibitor of Drp1 reduced renal tubular cell apoptosis and acute kidney injury.

TITLE: Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models

AUTHOR CONTACT:
Zheng Dong
Medical College of Georgia, Augusta, Georgia, USA.
Phone: (706) 721-2825; Fax: (706) 721-6120; E-mail: zdong@mail.mcg.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=37829


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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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