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: email@example.com.
First published October 7, 2019 - More info
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.
A subscription is required for you to read this article in full. If you are a subscriber, you may sign in to continue reading.
Click here to sign into your account.
Please select one of the subscription options, which includes a low-cost option just for this article.
If you are at an institution or library and believe you should have access, please check with your librarian or administrator (more information).
Please try these troubleshooting tips.