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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.
The number of patients with chronic kidney disease (CKD) and hypertension is increased with age; however, it is not clearly defined why and how aging causes renal dysfunction and hypertension. Nuclear factor of activated T-cells 5 (NFAT5) is a transcription factor that is activated upon hypertonic conditions as observed in the renal medulla. Genome-wide association study has suggested that NFAT5 variants are associated with the elevation of blood pressure and serum sodium levels. We have shown that the renal tubular cell-specific NFAT5 conditional knockout (cKO) mice exhibit salt-sensitive hypertension, while the mice exhibit impaired urine concentrating ability and are susceptible to renal fibrosis. These phenotypes resemble aging-associated renal dysfunction, i.e., urine concentrating disorder, salt-sensitive hypertension, and renal fibrosis. We therefore investigated the possible involvement of NFAT5 in aging-related changes of the kidney.
To evaluate age-related changes in NFAT5 activity, we used NFAT5-luciferase transgenic (NFAT5-luc TG) mice, which enable in vivo visualization of NFAT5 activity. Kidneys from wild type (WT) mice at 3, 6, 12, and 18 months of age were analyzed for mRNA expressions of Nfat5, cell senescence markers (p21, p16), senescence-associated secretory phenotype (SASP) factors (Il-6, Mmp3, Icam1, Serpine1), and fibrosis markers (Tgfb1 and Col1a1) by real-time quantitative PCR. Renal function, fibrosis (Azan staining), gene expressions of SASP-related factors, and immunostaining for p21 were compared between WT and cKO mice at 3 and 18 months.
NFAT5 activity in the kidney significantly increased in 23-month-old NFAT5-luc TG mice compared with 5-month-old mice. In WT mice, mRNA expression of p21, p16, Il-6, Mmp-3, and Serpine1 increased or tended to increase with aging up to 18 months, whereas Icam1, Tgfb1, and Col1a1 showed no clear changes. At 18 months, cKO mice exhibited marked renal atrophy, advanced interstitial fibrosis on Azan staining, and significantly higher serum creatinine levels than age-matched WT mice. The mRNA expressions of p21, p16, Il-6, and Mmp3 tended to be higher in cKO mice than in WT mice at 3 months, and all markers tested were significantly elevated in cKO mice compared with WT at 18 months. Immunostaining for p21 revealed more widespread expression of p21 in tubular cells in cKO mice compared with WT mice at 18 months of age.
Renal tubular NFAT5 deficiency promotes premature renal aging, fibrosis, and functional decline, which is accompanied by upregulation of SASP and profibrotic factors. In contrast, NFAT5 activity increases with normal aging, suggesting that NFAT5 functions as a protective factor maintaining renal homeostasis in the elderly.
