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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.
Chronic hyperglycemia contributes to the development of diabetic microvascular complications, with diabetic nephropathy (DN) being the most prevalent and a major cause of morbidity and mortality. Prolonged high glucose exposure activates multiple stress pathways in renal cells, leading to hemodynamic and metabolic disturbances. While current therapies manage hypertension and hyperglycemia, they fail to address residual renal risk, underscoring the need for novel therapeutic targets. Mitochondrial dysfunction and impaired nutrient-sensing pathways have emerged as critical contributors to DN. Given the importance of mitochondria in renal homeostasis, this study investigates mitochondrial quality control (MQC) mechanisms—particularly mitophagy and mitochondrial proteases—in type 1 diabetic nephropathy, and evaluates potential therapeutic agents to restore mitochondrial integrity.
We employed streptozotocin (STZ)-induced type 1 diabetic nephropathy in rats and high-glucose (30 mM) exposure in NRK-52E cells to model DN.
In vitro: NRK-52E cells were treated for 48 h with glucose (30 mM) alone or co-incubated with myo-inositol (5/10 µM), palmitoylethanolamide (PEA; 0.375/1.5 µM), or beta-aminoisobutyric acid (100/200 µM). Protein expression was assessed using western blot and immunofluorescence.
In vivo: STZ (55 mg/kg, i.p.) was administered to induce diabetes. After 4 weeks, diabetic rats were treated with myo-inositol (37.5/75 mg/kg) for another 4 weeks. Renal function markers (BUN, creatinine, albuminuria) were measured, and kidney tissues were analyzed for mitochondrial and autophagy-related proteins via western blot and immunohistochemistry.
High-glucose exposure significantly reduced expression of antioxidant proteins, mitophagy markers, and mitochondrial biogenesis proteins in NRK-52E cells and diabetic rat kidneys. Myo-inositol treatment ameliorated albuminuria, improved renal function, and restored mitophagy by upregulating the PINK1/Parkin pathway, along with mitophagy receptors PHB2 and NIX. It also enhanced mitochondrial biogenesis via the NRF2/SIRT1/PGC-1α axis. PEA restored mitochondrial protease LONP1 and improved mitochondrial biogenesis in high-glucose-exposed cells. Similarly, beta-aminoisobutyric acid treatment upregulated LONP1 and mitochondrial biogenesis markers, indicating protective effects on MQC under hyperglycemic stress.
Hyperglycemia impairs mitochondrial quality control in renal cells, contributing to diabetic nephropathy. Myo-inositol, PEA, and beta-aminoisobutyric acid demonstrated mitochondrial protective effects by enhancing mitophagy, mitochondrial biogenesis, and protease function. These findings support MQC pathways as promising therapeutic targets in DN and suggest the utility of metabolic and mitochondrial modulators in preserving renal function in diabetes.
