Linking transcription to energy: the path to understand kidney injury

The metabolic impairment of kidney tubular cells is a key mechanism underlying the pathophysiology of renal fibrosis. In particular, a drastic reduction in fatty acid oxidation is essentially responsible for the global energy failure occurring in the tubulointerstitial compartment. Piret et al. propose a novel transcriptional regulatory mechanism involving the decrease in the expression of Krappel-like factor 15 in proximal tubular cells after kidney injury, which results in a major derangement of fatty acid oxidation. Copyright (C) 2021, International Society of Nephrology. Published by Elsevier Inc. All rights reserved.

Automated summary

The metabolic impairment of kidney tubular cells plays a key role in the pathophysiology of renal fibrosis, with a drastic reduction in fatty acid oxidation being a major factor contributing to global energy failure in the tubulointerstitial compartment. Additionally, the decreased expression of Krappel-like factor 15 in proximal tubular cells after kidney injury may further disrupt fatty acid oxidation.