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PRECLINICAL PUBLICATION · 2018

TAK1 mediates excessive autophagy via p38 and ERK in cisplatin-induced acute kidney injury.

Mouse / Chemical/toxin

Evidence by therapy association

Study details and outcomes are extracted in the context of a specific intervention. Separate associations are retained rather than silently merged.

PMID 29504713 ↗2018Reported benefit

TAK1 mediates excessive autophagy via p38 and ERK in cisplatin-induced acute kidney injury.

MouseChemical/toxinBALB/cMalen = 6 per group for in vivo endpoints; total animal number not…Intraperitoneal5Z-7-oxozeaenol 4 mg/kg; 3-methyladenine 20 mg/kg per day;…First injection 1 hour before cisplatin

Model: Cisplatin-induced acute kidney injury, with cisplatin dissolved in 0.9% saline at 1 mg/mL and given at 20 mg/kg by intraperitoneal injection, and animals killed 72 hours later

TAK1 inhibition lowered serum creatinine and urea nitrogen, reduced tubular damage, decreased LC3II and restored p62, and reduced p38 and ERK phosphorylation after cisplatin.

Extraction: extract · Supplied extraction confidence: 0.85. Machine-extracted fields require source verification.