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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 revealed that interactions between autonomic nervous activity and immune cells play crucial roles in both the progression and suppression of various diseases. Among these, vagus nerve stimulation (VNS) has been reported to exert organ-protective effects in multiple disease models by modulating immune cell function. The core concept underlying this neuroimmune interaction is the cholinergic anti-inflammatory pathway (CAP). When the vagus nerve is stimulated, released acetylcholine binds to nicotinic acetylcholine receptors—particularly α7nAChR—on macrophages, inducing an anti-inflammatory phenotype that suppresses inflammation and protects organs. In the kidney field, activation of VNS/CAP was first reported to provide renoprotective effects against ischemia–reperfusion injury (IRI)-induced acute kidney injury (AKI), and its downstream mechanisms have been extensively investigated. However, the effects of VNS on chronic kidney disease (CKD) remain largely unknown. A major obstacle has been the invasiveness of conventional VNS, which requires anesthesia, skin incision, nerve exposure, and electrode placement for each session, often resulting in tissue adhesion and poor reproducibility.
To overcome these limitations, we developed a minimally invasive system enabling repeated VNS under awake conditions. Optogenetics, a technique that allows neural control by light stimulation, was applied. We used ChATCre-ChR2 mice, in which the blue light-sensitive channelrhodopsin-2 (ChR2) was specifically expressed in efferent vagal fibers. A miniature blue LED was implanted adjacent to the cervical vagus nerve, and the lead wire was routed subcutaneously to a head-mounted infrared receiver. By transmitting infrared signals externally, we achieved “repetitive,” “awake,” and “remote-controlled” optogenetic VNS.
The effectiveness of this system was verified by recording vagus nerve activity during light stimulation. We then applied this technique to a unilateral ureteral obstruction (UUO) mouse model of renal fibrosis. Daily optogenetic VNS (5 Hz, 10 min) was performed for 7 days. Quantitative PCR analysis revealed decreased expression of fibrotic marker genes (Acta2, Tgfb1, Col1a1, Col3a1, Fn1). Histological analysis with Picrosirius Red staining demonstrated a marked reduction in fibrotic area, indicating significant attenuation of renal fibrosis.
This newly established system enables noninvasive, reproducible evaluation of chronic VNS and its long-term effects. Moreover, the system can be adapted not only to the vagus nerve but also to other peripheral nerves, including renal sympathetic and splenic nerves. In this presentation, we will introduce the technical details of this system and discuss the molecular mechanisms and downstream pathways through which VNS suppresses renal fibrosis.
