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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Aging research seeks to extend healthy life expectancy, and preserving renal function is crucial for sustaining vital physiological processes. However, the mechanisms underlying age-related renal decline remain unclear. In the kidney, inflammation triggered by viral proteins or drugs releases cytokines that contribute to renal injury. This study aimed to examine how the senolytic drugs dasatinib and quercetin (DQ), known for their rejuvenating properties, influence the expression of inflammation- and fibrosis-related genes in the kidneys of aged mice.
Mice were divided into five groups based on age and treatment with or without DQ administration: Young mice (4–6 months old); Aged mice (23–24 months old, n=10); DQ-treated Aged mice (Aged+DQ, 23–24 months old); Old mice (26–30 months old); and DQ-treated Old mice (Old+DQ, 26–30 months old). Expression levels of inflammation-related genes in kidney tissue were analyzed using quantitative real-time PCR (qRT-PCR) and DNA microarrays. Total RNA extracted from four mouse kidneys per group was pooled for microarray analysis. Additionally, paraffin-embedded kidney sections were stained with periodic acid–Schiff (PAS), Masson’s trichrome (MT), and immunohistochemical staining to evaluate pathological changes and quantify fibrosis.
In the microarray analysis comparing young vs. aged and young vs. old mice, 1,122 upregulated and 523 downregulated genes were identified. Pathway analysis revealed increased expression of inflammatory signaling and T-cell activation genes in immune cells of both aged and old mice.
qRT-PCR analysis of key senescence markers, inflammatory cytokines, chemokines, and macrophage markers indicated that gene expression increased with advancing age. Further analysis showed that DQ administration suppressed the expression of Ccl7 and Mmp7, genes associated with renal fibrosis. MT staining demonstrated increased fibrosis in old mice, which was reduced by the senolytic drug DQ. Immunohistochemical staining for the aging marker p16 revealed p16-positive senescent cells predominantly around the glomeruli. While p16 expression did not significantly increase in aged mice, it was markedly elevated in old mice and was suppressed by DQ treatment. Staining for the fibrosis marker SMA and the proximal tubule marker NHE3 showed enhanced fibrosis and decreased proximal tubule formation in aged and old mice; however, these changes were not reversed by DQ. Additionally, the macrophage marker Iba1 exhibited a pronounced increase in old mice that was not improved by senolytic treatment.
Our findings indicate that tissue aging in naturally aged mice advances primarily through inflammatory processes in the kidney. A comparison between aged and old mice revealed a pronounced increase in inflammatory responses in the latter. Comprehensive analysis suggests that suppression of inflammation is a principal mechanism underlying the renoprotective action of senolytic drugs. The reduction of inflammatory cytokine secretion appears to be a key process contributing to the kidney-protective effects of DQ.
