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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 one of the most prevalent and severe microvascular complications of diabetes, serving as the leading cause of end-stage renal disease (ESRD). Mitochondrial dysfunction in renal tubular epithelial cells is a critical mechanism driving the onset and progression of DKD. Maintaining mitochondrial integrity is essential for protecting renal tubular function and slowing disease progression. This study aims to explore whether the HNF4α/BNIP3/ANXA5 signaling axis plays a critical role in maintaing mitochondrial quality of tubular epithelial cells and alleviating DKD.
The db/db diabetic mouse model and high glucose-treated renal tubular epithelial cell (RTEC) model were employed. Levels of HNF4α, BNIP3 and ANXA5 were detected using immunohistochemistry, western blot, qPCR and other techniques. Mitochondrial function was evaluated by measuring by the mitochondrial membrane potential (MMP), ROS levels, ATP production and mitophagy activity. Gene gain- and loss- function experiments were conducted to elucidate the roles of candidate genes in the HNF4α/BNIP3/ANXA5 axis in preserving mitochondrial quality.
The mitochondrial quality in RTECs was significantly decreased in DKD, associated with the decrease of HNF4α, BINP3 and ANXA5. In vitro experiments showed that overexpression of HNF4α significantly increased the expressions of BNIP3 and ANXA5, leading to improved mitochondrial quality, evidenced by enhanced mitophagy, increased MMP and ATP levels, and reduced ROS accumulation. Conversely, knockdown of BNIP3 or ANXA5 partially abrogated HNF4α-mediated mitochondrial protection, suggesting that this signaling axis is crucial for mitochondrial quality control and contributes to the pathogenesis of DKD.
The HNF4α/BNIP3/ANXA5 signaling axis plays a key role in the development of DKD via regulating mitochondrial quality. Targeting this pathway may offer promising therapeutic strategies for the treatment of DKD.
