Journal
KIDNEY INTERNATIONAL
Volume 100, Issue 6, Pages 1165-1167Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.kint.2021.09.018
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Funding
- Spain's Ministerio de Ciencia e Innovacion [PID2019-104233RB-100/AEI/10.13039/501100011033]
- Federation of European Biochemical Societies (FEBS) Long-Term Fellowship
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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.
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.
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