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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.
Autophagy is a fundamental mechanism that maintains cellular homeostasis by degrading and recycling damaged organelles and cellular components. However, in chronic kidney disease (CKD), the autophagy-lysosomal pathway is suppressed or functionally impaired, leading to the accumulation of damaged mitochondria and proteins within cells, which induces oxidative stress and inflammatory responses, ultimately accelerating tubular injury and renal dysfunction. Transcription Factor EB (TFEB), a key regulator of autophagy and lysosomal biogenesis, is dysregulated in CKD, contributing to impaired autophagic flux and disease progression. This study evaluated whether the autophagy enhancer could restore autophagy-lysosomal pathway, reduce lysosomal stress, and exert renoprotective effects in a CKD model.
CKD was induced in C57BL/6 mice by feeding adenine. The mice were divided into four groups: control, control+MSL-7, CKD, and CKD+MSL-7 (n = 7–8 per group). We used MSL-7 (25 mg/kg/day IP, LysoTech, Korea) which activates TFEB, thereby promoting autophagy and restoring autophagy-lysosomal function. Renal function was assessed using serum BUN and cystatin C levels. Kidney tissues were analyzed for tubular injury and fibrosis using Periodic Acid-Schiff staining, Masson’s Trichrome staining and alpha-SMA immunohistochemistry. TFEB expression and nuclear translocation, along with expression levels of p62, LC3 and LAMP1, were examined using qPCR, Western blot and immunostaining. Statistical significance was determined by one-way ANOVA followed by Tukey’s post hoc test.
CKD mice exhibited significantly elevated BUN and cystatin C levels compared to controls (p < 0.001), which were reduced after MSL-7 treatment, indicating improved renal function (p < 0.05). In CKD kidneys, marked tubular dilatation, increased fibrosis, and elevated α-SMA were observed compared to the control (p < 0.001), they were reduced after MSL-7 treatment (p < 0.05). Reduced TFEB expression in CKD evaluated by qPCR, Western blot and IF was recovered by MSL-7. IF analysis revealed an accumulation of both p62 and LC3 in CKD compared to controls, indicating the accumulation of autophagosomes. Following MSL-7 treatment, the accumulation of p62 and LC3 was significantly reduced (p < 0.01), suggesting restoration of autophagic flux. Western blot analysis showed that compared to controls, CKD exhibited increased p62 levels and a decreased LC3-II/LC3-I ratio, indicating increased autophagosome accumulation and impaired autophagosome degradation, resulting in overall suppression of autophagic flux. These alterations were reversed by MSL-7 treatment, confirming recovery of autophagic function (p < 0.05). Decreased LAMP1 expression in CKD compared to control was restored by MSL-7 which was confirmed by qPCR, Western blot, and IF (p < 0.05).
This study shows that MSL-7 activates TFEB to restore the autophagy-lysosomal pathway and alleviates lysosomal stress, inflammation and fibrosis in a CKD model, suggesting that autophagy enhancer is a promising therapeutic strategy for CKD.
