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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.
Diabetic nephropathy (DN) remains a leading cause of end-stage renal disease worldwide, driven by complex metabolic and inflammatory disturbances. Mitochondrial dysfunction is increasingly recognized as a central mechanism in DN progression, yet therapeutic strategies directly targeting mitochondrial signaling remain limited. Recent discoveries have identified mitochondrial-derived micropeptides, such as MOTS-c, as regulators of cellular metabolism and stress responses. However, their role in renal pathophysiology has not been fully explored. The goal of this research is to investigate the protective role of MOTS-c in diabetic nephropathy and assess whether exogenous MOTS-c administration could mitigate renal injury by modulating mitochondrial biogenesis and inflammatory pathways, which can introduce a new mitochondrial-targeted therapeutic strategy for DN management.
A multi-tiered approach was employed in this research, integrating in vitro and in vivo analyses. Human renal proximal tubular epithelial cells (HK-2) were exposed to high-glucose conditions to induce diabetic-like injury, followed by MOTS-c treatment. Mitochondrial function was assessed using Seahorse XF analysis, while gene expression of PGC-1α, NRF1, and inflammatory cytokines (IL-6, TNF-α) was quantified by qPCR and Western blotting. In parallel, streptozotocin-induced diabetic mice received subcutaneous MOTS-c or placebo for 8 weeks. Renal function was evaluated through serum creatinine, urinary albumin-to-creatinine ratio (ACR), and histopathological scoring.
The results showed that MOTS-c treatment restored mitochondrial respiratory capacity in glucose-stressed HK-2 cells, significantly increasing ATP production and reducing mitochondrial ROS levels by 40%. Expression of PGC-1α and NRF1 rose by 2.3-fold, while IL-6 and TNF-α expression decreased by 55% and 47%, respectively. In diabetic mice, MOTS-c administration lowered serum creatinine by 28%, reduced urinary ACR by 42%, and preserved glomerular architecture compared to controls. Electron microscopy revealed improved mitochondrial density and cristae structure within renal tubular cells.
In conclusion, these findings show that MOTS-c can exert renoprotective effects through mitochondrial restoration and inflammation suppression, highlighting its potential as a therapeutic candidate for diabetic nephropathy. This research opens the way for targeted mitochondrial therapeutics in nephrology, with future work focusing on clinical translation and optimization of MOTS-c analogs with enhanced renal bioavailability.
