Commentary 10.1172/JCI131171

DNA damage response protects against progressive kidney disease

Bruce A. Molitoris

Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Address correspondence to: Bruce A. Molitoris, Research-2, Room 266, 950 West Walnut Street, Indianapolis, Indiana 46202, USA. Phone: 317.274.1251; Email: bmolitor@iu.edu.

Find articles by Molitoris, B. in: JCI | PubMed | Google Scholar

First published October 7, 2019 - More info

Published in Volume 129, Issue 11 on November 1, 2019
J Clin Invest. 2019;129(11):4574–4575. https://doi.org/10.1172/JCI131171.
© 2019 American Society for Clinical Investigation
First published October 7, 2019 - Version history

The pathophysiology of cellular injury and repair has been extensively studied in acute kidney injury (AKI) for more than 70 years. Although a great deal of knowledge has been generated, a debate over the importance of repairing damaged cells versus replacing them by proliferation remains. In this issue of the JCI, Kishi et al. demonstrate that following kidney epithelial cell injury, DNA repair, rather than cell proliferation, plays the central role in recovery and longevity by minimizing apoptosis, G2/M cell-cycle arrest, and subsequent fibrosis. This has important therapeutic implications and highlights the need for more sensitive techniques to evaluate functional, structural, and molecular recovery following injury.

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