March 3, 2026Open Access

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.

Abstract

TIMP2 is upregulated in injured renal tubules and promotes maladaptive repair and cell senescence. Genetic deletion of TIMP2 in tubular epithelial cells attenuates renal fibrosis and improves mitochondrial function. TIMP2 activates Wnt/β-catenin signalling by binding to LRP6 via an MMP-independent mechanism.

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

Key Points

Abstract

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