Activation of branched chain amino acid catabolism protects against nephrotoxic acute kidney injury

2024/12/20 by Stephen J. DiMartino, Mónica P. Revelo, Sandeep K. Mallipattu +1 · 1 voice
Medicine · Pharmacology, Toxicology and Pharmaceutics · #Drug-Induced Hepatotoxicity and Protection #Nephrotoxicity and Medicinal Plants

paper · doi:10.1152/ajprenal.00260.2024

openalex publication_date 2024/12/20 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01

Abstract

This study explored the effects of pharmacological activation of branched chain amino acid (BCAA) catabolism using BT2 to prevent nephrotoxic acute kidney injury (AKI) in mice. Our results indicate that activation of BCAA catabolism protects against nephrotoxic AKI, in association with reduced BCAA accumulation, reduced mammalian target of rapamycin protein complex 1 signaling, and improved mitochondrial bioenergetics.

Citations

• Branched Chain Amino Acids
• Loss of proximal tubular transcription factor Krüppel-like factor 15 exacerbates kidney injury through loss of fatty acid oxidation

Discussions

• New AJP-Renal study explores effects of pharmacological activation of branched chain amino acid catabolism using BT2 to prevent nephrotoxic acute kidney injury in mice. Activation of BCAA catabolism p [bsky, 0 points, 0 comments]

Related

• Urinary Branched-Chain Amino Acid Excretion and Chronic Kidney Disease Progression in Patients With Type 2 Diabetes
• Branched Chain Amino Acids
• Defective branched chain amino acid catabolism contributes to cardiac dysfunction and remodeling following myocardial infarction
• Phosphoenolpyruvate carboxykinase 1-mediated cataplerosis is required to maintain mitochondrial fitness and to avoid kidney disease progression
• A Randomized Trial of Intravenous Amino Acids for Kidney Protection