TIMP2 promotes AKI‐CKD transition by inducing tubular maladaptive repair and cell senescence via targeting Wnt/β‐catenin signalling

Key Points

• Cell senescence occurs in injured renal tubules, driven by increased levels of TIMP2.
• Genetic deletion of TIMP2 significantly reduces renal fibrosis and enhances mitochondrial function.
• Analysis of TIMP2 shows it activates wnt/beta-catenin signalling, linking it directly to maladaptive repair.
• The findings indicate a potential target for preventing progression from acute kidney injury to chronic kidney disease.