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Podocyte aging and diabeticCellular senescence is portrayed as apermanent cease of cell cycle progreskidney disease by Li Li1,2,Youhua Liu is a book available to read on EtoBox.

What is Podocyte aging and diabeticCellular senescence is portrayed as apermanent cease of cell cycle progreskidney disease about?

Li Li1,2 and Youhua Liu1,2release of the senescence-associatedsecretory phenotype proteins.4,5 SenesPodocyte injury causes a series of cellular changes, includingcent podocytes lose slit diaphragm–associated proteins, secrete senescencehypertrophy, dedifferentiation, senescence, apoptosis, andassociated secretory phenotype comdetachment. Although evidence suggests a pivotal role of podocyteponents, upregulate senescence markerssenescence in diabetic kidney disease, the exact triggers andp53, p21Cip1, and p16INK4a, and expressunderlying mechanism remain elusive. In this study, Li et al. uncoveran increased senescence-associated bthat GPR124, a G-protein–coupled receptor, protects against podocytegalactosidase. These changes are furthersenescence by inhibiting focal adhesion kinase. These findingsexacerbated by an impaired autophagyand a disrupted mitochondrial homeounderscore that the GPR124/focal adhesion kinase axis could be astasis, which together lead to podocytenovel target for diabetic kidney disease therapy.dysfunction and proteinuria, therebyKidney International (2025) 107, 596–598; glomerular damage andCopyright a 2025, International Society of Nephrology. Published by

Author

Li Li1,2,Youhua Liu

Published

2025

Language

EN