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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.
Patients with chronic kidney disease (CKD) have a high prevalence of sarcopenia, which not only leads to reduced physical activity but also increases the risk of cardiovascular complications. Recently, myokines secreted from skeletal muscle during exercise have attracted attention for their potential role in metabolic regulation and muscle preservation. Among them, irisin, a myokine derived from FNDC5, has been reported to correlate with muscle mass and strength. Patients with CKD often show decreased circulating irisin levels, which may contribute to vascular endothelial dysfunction and the progression of atherosclerosis. Based on these findings, we hypothesized that decreased irisin may contribute to renal scarring processes through endothelial dysfunction. To test this hypothesis, we investigated the effects of exercise on irisin dynamics and assessed the role of irisin in the progression of renal injury in a mouse model of CKD.
We performed 5/6 nephrectomy on C57BL/6J mice as a model of uremic sarcopenia as reported previously and treated them with or without exercise intervention for 8 weeks. We examined changes in FNDC5 expression and circulating irisin concentrations, along with glomerular endothelial injury and renal impairment.
In CKD model mice, skeletal muscle mass and grip strength remained unchanged during the observation period. However, skeletal muscle expression of FNDC5 was significantly reduced compared to the sham group. Accordingly, decreased serum irisin levels, glomerular endothelial injury detected by glycocalyx staining, and glomerulosclerosis were observed. Exercise intervention improved FNDC5 expression and serum irisin levels in CKD mice. Furthermore, exercise prevented progressive renal dysfunction by improving reduced eNOS expression and protecting against glomerular endothelial injury.
Exercise-induced renal protection may be caused by irisin-mediated endothelial protection, and improved FNDC5 expression and irisin secretion suggest that these could provide novel therapeutic approaches for CKD patients with sarcopenia.
