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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.
Acute kidney injury (AKI) easily progresses to chronic kidney diseases and end-stage renal diseases. Renal ischemia-reperfusion injury (IRI) is an important cause of AKI. The pathogenesis of renal IRI is complex, and its pathological characteristics mainly include renal tubular epithelial cell injury and death. Apoptosis is one of the main mechanisms of hypoxia-induced renal tubular epithelial cell death. Autophagy regulates apoptosis and plays a key role in the development of renal IRI. FAK family-interacting protein of 200 kDa (FIP200) is a crucial component of the ULK-1-Atg13-FIP200 complex formed in mammalian cells upon autophagy induction. Our previous study in mouse macrophages found that FIP200 might regulate the nuclear translocation of HMGB1 via modifying its acetylation caused by infection. However, the precise mechanisms of FIP200 underlying HMGB1 in renal IRI-mediated AKI remain elusive.
The Billups hypoxic modular system (MIC-101, Billups-Rothenberg, USA) was used to establish the hypoxia/reoxygenation (H/R) cell model in HK2 cells. Cells were maintained under hypoxia for 5 min, 30 min, 45 min, 1 h, 2 h, 4 h, 6 h, and 24 h, and then reoxygenated for 24 h. Cells in the control group were not subjected to hypoxia then reoxygenation. All animal studies were approved by the Ethics Committee of Sichuan Provincial People’s Hospital (approval No. L201735). Twenty-four wild-type mice were divided into 8 groups, and the renal pedicles of their left kidney were clamped with microvascular forceps at 0 min, 15 min, 30 min, 45 min, 1 h, 2 h, 4 h, 6 h and 24 h, respectively, to determine a suitable timepoint of IRI. Then, 6 FIP200 conditional knockout mice in the renal tubular epithelial cell (FIP200loxp-/loxp- Ggt cre/mice, FKO mice), in parallel to 12 wild-type mice, were randomly divided into renal IRI group and sham operation group.
In this study, we found that the expression of the autophagy-related protein FIP200 was up-regulated in vivo and in vitro after renal IRI or hypoxia/reoxygenation (H/R). Mice with conditional FIP200 knockout in renal tubules (FIP200loxp-/loxp--Ggt cre/mice) showed severe renal tissue damage after IRI. Additionally, overexpression and knockdown of FIP200 in HK2 cells revealed its protective effects on H/R injury of renal tubular epithelial cells. Further, we confirmed that FIP200 could interact with HMGB1 by immunoprecipitation assays and biolayer interferometry. Hence, we speculate that FIP200 could induce autophagy by regulating the competitive binding of HMGB1 and autophagy-related factors.
Our data indicate that FIP200 has an important role in preventing renal tubular cell damage and death following renal IRI, and might be a novel potential target for prevention and treatment of AKI caused by IRI.
