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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.
Recent studies have shown that acute tubular injury and impaired mitochondrial fatty acid oxidation (FAO) are the key contributors to tubulointerstitial fibrosis (TIF) in cisplatin-induced nephropathy (CIN). Fortunately, the effective treatments for CIN using Chinese herbal medicine are available in China. Among these, Abelmoschus manihot (AM), a medicinal plant, has been widely reported to be used for treating acute tubular injury in CIN. Notably, AM-derived extracellular vesicle-like particles (AMEVLPs) as a newly isolated bioactive component has received considerable attention, but its therapeutic mechanisms by which AMEVLPs alleviate acute tubular injury and associated TIF in CIN remain unclear. Therefore, this study aims to clarify the therapeutic effects of AMEVLPs, a natural advanced delivery system derived from AM, on acute tubular injury and TIF in CIN, along with the underlying therapeutic mechanisms.
Differential centrifugation and ultracentrifugation were used to isolate AMEVLPs from AM. Transmission electron microscopy (TEM), flow nano analyzer, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), agarose gel electrophoresis, and thin-layer chromatography were employed to characterize AMEVLPs. In this study, rats were treated with PBS, AMEVLPs or empagliflozin (EM), via gavage for 8 days. A single cisplatin injection on days 6-8 was used to establish CIN rat models. Renal function, kidney pathology, and the markers of acute tubular injury and TIF were assessed for renal damage evaluation, respectively. For mechanistic exploration, mitochondrial FAO, mitochondrial morphological alterations, ATP production and mitochondrial mass proteins were detected in vivo. Mitochondrial membrane potential and reactive oxygen species (ROS) production were investigated in vitro.
We found that AMEVLPs significantly improved renal structural integrity, restored renal function, and reduced renal tubular injury and TIF. AMEVLPs demonstrated superior therapeutic effects over EM in certain indicators. Additionally, AMEVLPs enhanced mitochondrial FAO in the kidneys by upregulating the key FAO enzyme, carnitine palmitoyltransferase 1A (CPT1A). Mechanistically, AMEVLPs improved mitochondrial homeostasis, as evidenced by the restoration of mitochondrial structure, increased mitochondrial mass and ATP production, inhibition of oxidative stress, and enhanced mitochondrial membrane potential. These effects collectively contributed to the improvement in mitochondrial FAO and the attenuation of cisplatin-induced acute renal tubular injury and TIF.
In this study, we successfully isolated high-quality AMEVLPs and demonstrated that AMEVLPs, different from EM, accurately improve acute tubular injury and TIF in CIN, and that underpinning therapeutic mechanisms are closely related to restoring CPT1A mediated tubular epithelial cell mitochondrial fatty acid oxidation. Our findings provide new pharmacological evidence for using AMEVLPs as an advanced delivery system for treating CIN.
