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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.
Autotaxin (ATX), an enzyme that converts lysophosphatidylcholine into lysophosphatidic acid (LPA), which promotes cell migration and proliferation and plays a key role in fibrogenesis. Although ATX has been explored in kidneys, the therapeutic implications and precise molecular mechanisms underlying ATX inhibition in chronic kidney disease (CKD) remain insufficiently characterized. Accordingly, this study aimed to elucidate the therapeutic potential of ATX inhibition in CKD. In this study, we investigated the antifibrotic effects of an ATX inhibitor (ATXi) in CKD.
This study used a folic acid (250 mg/kg IP)-induced CKD model to test the renoprotective effects of ATXi (30 mg/kg/day PO) over 21 days. Mice were divided into three groups: control, CKD, and CKD+ATXi. Renal ATX expression and extracellular matrix deposition were assessed using immunohistochemistry (IHC). Renal function was evaluated by measuring blood urea nitrogen (BUN) and cystatin C. Urine LPA levels were quantified using an ELISA. Kidney pathology was examined using periodic acid-Schiff, Masson’s trichrome. Mitochondria was examined using electron microscopy. Lipid accumulation was assessed via Oil Red O staining. Finally, gene and protein expressions of LPA receptors and other targets were analyzed using qPCR and IHC.
BUN and cystatin C were elevated in CKD group compared with the controls, whereas treatment with ATXi markedly reduced these levels, indicating improved renal function. Histological analysis revealed increased tubular dilatation and interstitial fibrosis in the CKD group, both of which were significantly alleviated by ATXi treatment. The expression levels of α-SMA, COL1α1, and Ki67 were markedly upregulated in the CKD group compared with the controls, but were significantly reduced following ATXi treatment. Electron microscopy revealed a decreased number of mitochondria with intact cristae in CKD kidneys, which was restored by ATXi treatment. To determine which LPA receptors (LPA1–6) were affected by ATX inhibition, mRNA expression and lipid accumulation in the kidney were analyzed. The CKD group showed significantly elevated LPA1 and LPA6 expression accompanied by enhanced lipid accumulation, whereas ATXi treatment suppressed lipid deposition and reduced LPA1 and LPA6 mRNA levels. Collectively, these findings demonstrate that ATX inhibition ameliorates CKD, highlighting ATX as a potential therapeutic target for renal fibrotic diseases.
This study provides evidence that ATXi improves fibrosis in CKD through the blockade of the LPA signaling pathway, suggesting that ATX inhibition may serve as a potential therapeutic strategy in renal fibrotic diseases.
