What is it about?
Albuminuria is the hallmark of nephrotic syndrome (NS), a leading cause of chronic kidney disease affecting 500 million people worldwide. Thus, there is a clear need to discover novel drug targets to treat proteinuric kidney disease. We demonstrate that thioredoxin-interacting protein (TXNIP), a redox protein that forms the complex with antioxidant oxidoreductase thioredoxin (Trx), relocates from nucleus to mitochondria when C/EBP homologous protein (CHOP), a major endoplasmic reticulum (ER) stress-associated transcription factor, is induced by albuminuria. TXNIP shuttling to mitochondria is essential for mitochondrial reactive oxygen species (ROS) production, which oxidizes mitochondrial-specific Trx2 and disrupts the association between Trx2-TXNIP and Trx2-ASK1 in mitochondria, leading to NLRP3 inflammasome activation and mitochondria-dependent apoptosis. Thus, TXNIP is a potential target to treat NS.
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Why is it important?
TXNIP is a potential target to treat nephrotic syndrome.
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This page is a summary of: Blocking CHOP-dependent TXNIP shuttling to mitochondria attenuates albuminuria and mitigates kidney injury in nephrotic syndrome, Proceedings of the National Academy of Sciences, August 2022, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2116505119.
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