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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.
Skeletal muscle wasting is closely linked to chronic kidney disease (CKD), a pathological change that impairs physical performance and worsens patient outcomes. We previously demonstrated that targeted myostatin inhibition via Antisense Oligonucleotides (ASO) counteracts CKD-induced activation of the myostatin/atrogin-1/MuRF-1 pathway, thereby improving muscle mass and function. Despite extensive research, it is still uncertain how myostatin inhibition alters the muscle fiber-type profile.
In our previous study, to generate a CKD model, male C57BL/6J mice were subjected to a 0.2% adenine-supplemented diet for 4 weeks, followed by 8 weeks of weekly subcutaneous treatment with saline, low-dose ASO (25 mg/kg), or high-dose ASO (50 mg/kg). Muscle mass, myofiber size, treadmill endurance, and grip strength were assessed, and muscle gene/protein expression was analyzed by qPCR and Western blotting. In the extension phase of this research, to evaluate fiber type distribution, tibialis anterior (TA) muscle sections were immunostained using BA-D5 (Type 1), SC-71 (Type 2a), and BF-F3 (Type 2b) antibodies, followed by quantification of the percentage of each fiber type using ImageJ.
Our previous study demonstrated that myostatin-targeted ASO therapy led to significant gains in muscle weight, size, and strength in CKD mice, accompanied by the attenuation of myostatin signaling and its downstream effectors, atrogin-1 and MuRF-1. Our immunofluorescence data revealed that 1) no Type 1 fibers are present in TA muscles, and 2) CKD promoted a pronounced reduction in oxidative Type 2a fibers along with a compensatory increase in glycolytic Type 2b fibers. ASO-treated mice showed a marked recovery of Type 2a fibers with a corresponding decrease in Type 2b fibers. These findings indicate that myostatin inhibition promotes a shift toward oxidative fiber restoration.
Myostatin inhibition not only attenuates muscle wasting but also enhances oxidative fiber recovery in CKD-associated sarcopenia. This suggests an additional mechanism through the improvement of muscle quality and metabolic phenotype. Ongoing studies, including Succinate dehydrogenase (SDH) staining and PGC-1α analysis, will further clarify the effects of myostatin inhibition on mitochondrial oxidative metabolism.
