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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) is a life-threatening condition with high morbidity and mortality. Despite substantial progress in understanding the mechanism of AKI, no effective therapies are available for treatment. We previously found that DcR2 is highly expressed in senescent renal tubular cells in patients with AKI and is associated with poor renal prognosis, indicating that targeted intervention of DcR2 may be an effective treatment for AKI.
DcR2-GFP transgenic mice, proximal tubular epithelial cell (PTEC) DcR2 conditional knockout CKO (DcR2-CKO) mice were constructed. Moderate (25 min) and severe ischemia (35 min) reperfusion (IR)-induced AKI models were used to investigate the role of DcR2 in kidney injury. Four-dimensional quantitative proteomics, bioinformatics analysis and validation studies were conducted to explore the underlying mechanism. The antagonistic peptides of DcR2 (AP-D) using Ph.D.-12 phage display library were screened, and the effects of AP-D in AKI was demonstrated in vivo and in vitro experiments.
DcR2 expression was abnormally increased in renal tubules in patients of AKI, and associated with poor renal prognosis. Similar results were found in moderate and severe IR injury mouse models. DcR2-GFP transgenic mice verified that DcR2 was specifically expressed in PTECs and associated with kidney injury. DcR2-CKO improved kidney injury, inhibited cell senescence, promoted cell proliferation and regeneration, and repressed renal fibrosis. Similar results were found in hypoxia/reoxygenation-treated primary PTECs. Four-dimensional proteomics showed that DcR2 modulated tubular senescence by regulating Hmgcs2 (a rate-limiting enzyme of endogenous ketogenesis) expression, thereby affecting renal beta-hydroxybutyrate (β-OHB) levels. Hmgcs2 inhibition or deletion promoted tubular senescence by depleting β-OHB. Nevertheless, β-OHB administration ameliorated these phenomena. Moreover, PTEC-specific DcR2/Hmgcs2 double deletion inhibited Foxo3a by regulating histone acetylation, thereby boosting senescence. We screened out 10 antagonistic peptides of DcR2 (AP-D) using Ph.D.-12 phage display library, and found AP-D8 had the strongest proliferative effect. And AP-D8 effectively inhibited renal interstitial fibrosis and tubular senescence, thereby alleviating AKI.
DcR2 promotes kidney injury and tubular senescence by regulating Hmgcs2-induced β-OHB, and AP-D8 targeted intervention for DcR2 alleviates acute kidney injury. Collectively, these results imply that DcR2 is a promising therapeutic target for treating AKI.
