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Tubular senescence is a major determinant of chronic kidney disease and identification of potential therapeutic targets involved in senescent tubular epithelial cells has clinical importance. Our findings indicate that LAPTM5 contributes to tubular senescence at least in part through inhibiting WWP2-mediated ubiquitination of NICD1, followed by inducing of SASP, finally causing kidney injury in CKD. Genetic or pharmacological targeting of LATPM5 may provide a novel approach for the treatment of CKD.
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This page is a summary of: Lysosomal-Associated Protein Transmembrane 5, Tubular Senescence, and Progression of CKD, Journal of the American Society of Nephrology, July 2024, Wolters Kluwer Health,
DOI: 10.1681/asn.0000000000000446.
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