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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 the most common case of chronic kidney disease (CKD) globally and remains a major cause of end-stage renal disease. The molecular mechanisms underlying senile DKD development have been widely explored but the therapeutic strategies are still limited. Total flavone of Abelmoschus manihot (TFA), a natural extract, has been applied extensively for treatment of proteinuria in the patients with early diabetic kidney disease (DKD) in China. However, its therapeutic mechanisms remained elusive. Recently, the increasing evidence has been indicated that endoplasmic reticulum (ER) and mitochondrial dysfunction play fundamental roles in the pathogenesis of DKD. The IP3R1-GRP75-VDAC1 signaling pathway orchestrates ER-mitochondria coupling, which plays an essential role in Ca²⁺ transfer and mitochondrial homeostasis. This study thereby aimed to investigate effects and mechanisms in vivo and in vitro of TFA on podocyte damage, compared with empagliflozin (EMPA), a novel therapeutic agent that inhibits proteinuria in the clinic, by modulating GRP75-dependent ER-mitochondria coupling and Ca²⁺-mediated apoptotic signaling.
The modified DKD rat models were subjected to uninephrectomy, intraperitoneal injection of streptozotocin (STZ), and a high-fat diet (HFD). The animals received either TFA, EMPA, or vehicle for 8 weeks. In vivo, proteinuria, renal function, kidney histopathology, and podocyte injury and apoptosis were evaluated, respectively. For in vitro experiments, murine podocytes were exposed to high-glucose (HG) conditions and treated with TFA, EMPA, or the cytosolic Ca²⁺ chelator BAPTA-AM, and subjected to GRP75 plasmid transfection. Confocal microscopy, fluorescent probes, and flow cytometry were used to assess ER-mitochondria colocalization, mitochondrial Ca²⁺ levels, mitochondrial membrane potential (ΔΨm), mitochondrial ROS (mtROS), and apoptosis. Western blotting and immunofluorescence were performed to determine the expression levels of IP3R1, GRP75, VDAC1 and apoptosis-related proteins.
For the modified DKD model rats, TFA and EMPA improved proteinuria, renal function, kidney histopathology, and podocyte injury and apoptosis in varying degrees, respectively in vivo. In vitro, TFA significantly downregulated the expression of IP3R1, GRP75 and VDAC1, restored Ca²⁺ homeostasis in podocytes, stabilized ΔΨm, reduced mtROS production, and inhibited podocyte apoptosis. It is noted that these beneficial effects in vivo and in vitro of TFA were comparable to or superior to those of EMPA.
We confirmed in this study that TFA, similar to EMPA, can ameliorate DKD by modulating GRP75-dependent ER-mitochondria coupling, thereby restoring mitochondrial homeostasis and preventing Ca²⁺-induced apoptosis in podocytes. This study suggests that GRP75 may serve as a potential therapeutic target for the treatment of DKD.
