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. 2021 May 9;13(5):1580. doi: 10.3390/nu13051580

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© 2021 by the author.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Renal injury alters proximal tubule cell metabolism by suppressing fatty acid oxidation and increasing anaerobic glycolysis. (A) Healthy proximal tubule (PT) cells relies utilization fatty acid oxidation by peroxisomes and mitochondria to generate ATP. Transcription factors such as PCG-1α and PPAR-α increase mitochondrial biogenesis and expression of genes related to fatty acid oxidation. Conversel y, glycolysis is not a big source of energy in the uninjured proximal tubule. Kidney injury impairs mitochondrial function and decreases expression of PGC-1α and PPAR-α (B). Therefore, fatty acid oxidation declines and injured PT cells rely on glycolysis to help meet energetic demands. Anaerobic glycolysis leads to increased levels of lactic acid. Created by BioRender.com.