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Abstract
Lysosomal transmembrane protein 5 (LAPTM5) is markedly upregulated in aged kidney models and correlates with renal senescence and fibrosis severity.
- Aging is associated with renal fibrosis driven by the senescence of renal tubular epithelial cells.
- LAPTM5 promotes the transformation of renal tubular epithelial cells by interacting with a specific protein and facilitating its degradation.
- This degradation relieves the inhibition of a signaling pathway involved in cellular recycling, leading to accelerated kidney fibrosis.
- Overexpressing a protein that counters LAPTM5 can reverse the fibrosis-inducing effects in renal tubular epithelial cells.
- A specific compound improves kidney function and reduces fibrosis in aging models by restoring cellular recycling processes.
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