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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.
Mammalian kidneys have a limited regenerative capacity. Although renal tubules can be repaired after injury, nephron loss due to kidney mass ablation or disease is never recovered in mammalian system. In this study, we investigated the de novo nephron regeneration after nephrectomy in axolotls, a model organism with remarkable regeneration ability.
Axolotls were subjected to unilateral 1/4 nephrectomy. Kidney tissues were collected and assessed at different time points (0, 1, 2, 4, 8, 12, and 16 weeks post-surgery). Histological and immunofluorescent analyses were performed to assess cellular repopulation, extracellular matrix (ECM) remodeling, and nephron formation. Proteomic profiling was used to study dynamic remodeling of ECM pathways.
We found that cells migrated into the resected sites and proliferated, starting at 1 week and reaching to more than 90% cell mass of the contralateral kidney at 4 weeks. Cell proliferation peaked between weeks 2 and 4 in the resected site and coincided with fibroblast activation, SOX9 expression and the induction of tenascin C (TNC). New glomeruli and mature tubules were formed by 12 weeks, indicating de novo nephrogenesis. Interestingly, TNC was transiently induced, peaking at 2 to 4 weeks post-injury, followed by gradual reduction. TNC knockdown significantly impaired cell proliferation and regenerative capacity. Notably, administration of TNC-derived peptide 6 (TCP6), a peptide recapitulating TNC function, accelerated ECM remodeling, advanced TNC induction, and accelerated nephron formation and functional maturation. RNA-seq analysis revealed that TCP6 treatment upregulates gene networks involved in wound healing, cell proliferation, and nephron development.
These findings provide strong evidence that functional nephrons can be de novo regenerated in the kidney of axolotls after partial nephrectomy. Tenascin C (TNC) is transiently induced and required for efficient cell proliferation and kidney regeneration. The TNC-derived matrikine TCP6 accelerates this process, highlighting the role of ECM signaling in kidney regeneration. These findings indicate that de novo nephron regeneration is achievable, identify TNC/TCP6 as potential accelerator of repair, and offer a framework for exploring regenerative pathways in mammalian kidneys.
