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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 kidney disease (DKD) is a leading cause of chronic kidney disease and end-stage renal disease, where early intervention is critical. The concept of “diabetic tubulopathy” highlights the pivotal role of renal tubular epithelial cells (RTECs) in DKD initiation and progression. Renal tubules are rich in mitochondria because of high energy demand, and mitochondrial dysfunction is recognized as a key driver of oxidative stress, apoptosis, and fibrosis in DKD. Among apoptotic regulators, voltage-dependent anion channel 1 (VDAC1) mediates cytochrome c (Cyt c) release and caspase activation, while our proteomic analysis identified elongation of very long chain fatty acids protein 5 (ELOVL5) as a differentially expressed protein with potential anti-fibrotic properties.
Hempseed, rich in polyunsaturated fatty acids, contains α-linolenic acid (ALA), which exhibits renal protective and anti-inflammatory effects. However, its impact on apoptosis and fibrosis in DKD is unclear. This study aimed to investigate whether ALA alleviates DKD-associated fibrosis by modulating the ELOVL5–VDAC1 signaling pathway.
A DKD model was established using db/db mice, which were randomly assigned to receive low- or high-dose hempseed extract (1.85g/kg/day or 3.7g/kg/day) or losartan (10 mg/kg/day) via oral gavage for 12 weeks. db/m mice receiving CMC-Na served as controls. Urine and serum samples were collected, and renal tissues were analyzed after treatment.
In vitro, HK-2 cells were exposed to high glucose (33.3 mM) and palmitic acid (0.2 mM) to mimic diabetic conditions, followed by treatment with ALA or PBS. Molecular docking and molecular dynamics simulations were performed to characterize the ALA–ELOVL5 interaction. ELOVL5 expression was silenced by siRNA, and a THR203 mutant was generated to assess the binding specificity of ALA. Mitochondrial membrane potential, morphology, and apoptosis markers were assessed to evaluate mitochondrial function and apoptosis.
ALA and hempseed extract exhibited significant therapeutic potential in DKD. Hempseed/ALA treatment significantly inhibited apoptosis and improved mitochondrial dysfunction in RTECs. ELOVL5 was identified as a potential target of ALA in DKD-associated fibrosis, and molecular dynamics simulations and site-directed mutagenesis confirmed THR203 as the key binding residue. ALA-induced upregulation of ELOVL5 inhibited VDAC1 activity, reduced Cyt c release–mediated apoptosis, and restored mitochondrial network integrity and membrane potential. In contrast, ELOVL5 silencing enhanced VDAC1-mediated apoptosis and abrogated ALA’s renal protective effects. These findings indicate that hempseed-derived ALA alleviates mitochondrial-dependent apoptosis through the ELOVL5–VDAC1 signaling pathway, exerting protective effects against DKD.
Hempseed-derived ALA counteracts mitochondrial-dependent apoptosis and renal fibrosis in DKD by modulating the ELOVL5–VDAC1 axis. These findings identify ELOVL5 as a novel regulator linking fatty acid to mitochondrial homeostasis and highlight ALA as a promising therapeutic candidate for DKD.
