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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.
Activating transcription factor 6 (ATF6), a key sensor of the unfolded protein response (UPR), is crucial for maintaining endoplasmic reticulum (ER) homeostasis and is implicated in various kidney diseases characterized by maladaptive UPR, known as ER stress. While ATF6’s role in renal physiology is recognized, its specific function in podocytes remains unclear. ATF6 has two isoforms, ATF6α and ATF6β, we generated podocyte-specific ATF6αβ conditional knockout mice (ATF6αβ cKO) to explore its role in podocyte homeostasis and glomerular injury.
To model glomerular injury, ATF6αβ cKO mice and wild-type (WT) littermates were treated with nephrotoxic serum to induce anti-GBM nephritis. Renal function was assessed from Days 0 to 21 by measuring urinary albumin-to-creatinine ratio (ACR). PAS staining and immunohistochemistry (IHC) were used to evaluate podocyte loss, and tubular damage. Gene expression analyses of UPR and ER-associated degradation (ERAD) pathways were performed via RT-qPCR and immunoblotting, focusing on ATF6 downstream targets including Derl3 and SDF2L1.
Under basal conditions, ATF6 αβ cKO mice exhibited no significant differences in renal function or glomerular architecture compared to WT controls. Following induction of anti-GBM nephritis, ACR peaked on day 4 after disease induction and gradually declined thereafter but did not return to baseline during the experimental period. The increased ACR were associated with podocyte damage (podocyte loss and decreased nephrin expression) and subsequent tubular damage. However, podocyte-specific ATF6αβ deficiency developed comparable levels of kidney dysfunction and podocyte damage, with no statistically significant differences observed. Notably, in WT mice, the expression of UPR sensors, PERK, IRE1, and ATF6, declined progressively during anti-GBM nephritis, reaching a nadir at Day 4. This was accompanied by a marked reduction in ERAD-related genes such as Derl3 and SDF2L1, which are responsible for clearing misfolded proteins. In contrast, in ATF6αβ cKO mice, podocyte-specific ATF6 deficiency led to a further decline in Derl3 and SDF2L1 expressions, indicating the contribution of podocyte ATF6 to the ERAD system, although it is dispensable for anti-GBM nephritis progression.
Our findings suggest that ATF6 signaling is not essential for maintaining baseline glomerular function or responding to acute podocyte injury at renal functional and histological levels. However, ATF6 may support ER quality control through ERAD during anti-GBM nephritis progression. Although dispensable under glomerular stress, podocyte ATF6 may enhance the ER stress responses, indicating an auxiliary yet functionally important role in maintaining proteostasis under pathological conditions. These results provide new insights into the ATF6-dependent adaptive mechanisms in podocyte injury.
This abstract was also submitted for the APCN × TSN 2025 Congress. By submitting the abstract to WCN 2026, the authors declare that re-submitting the abstract is permitted by the organizers of the previous meeting.
