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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.
Acute kidney injury (AKI) remains a major clinical problem with limited therapeutic options and a high risk of progression to chronic kidney disease. The kidney is densely innervated by sympathetic nerves, and adrenergic receptors are abundantly expressed in renal tubular cells—the primary site of injury in AKI—suggesting a critical role for sympathetic signaling in renal pathophysiology. However, the mechanisms underlying the cellular and metabolic protection provided by renal sympathetic modulation remain unclear. This study aimed to elucidate how selective activation of renal sympathetic nerves protects against AKI, focusing on mitochondrial metabolism and redox homeostasis.
To achieve selective sympathetic activation, dopamine β-hydroxylase (DbH)-Cre mice were crossed with channelrhodopsin-2 (ChR2) reporter mice, generating DbH-Cre/ChR2 mice expressing light-sensitive ion channels specifically in sympathetic neurons. Optical fibers were implanted around the renal artery, and blue light was delivered to activate renal sympathetic nerves. Extracellular recordings confirmed light-evoked action potentials, validating effective stimulation. Bilateral ischemia–reperfusion (I/R) injury was induced 24 hours after stimulation. Arterial pressure and renal blood flow were continuously monitored. Single-cell RNA sequencing (scRNA-seq) was performed to assess cell-type-specific transcriptomic changes. In vitro, human proximal tubular epithelial cells (HK-2) were exposed to hypoxia with or without norepinephrine to evaluate changes in neutrophil gelatinase-associated lipocalin (NGAL) expression, NAD⁺/NADH ratio, and mitochondrial respiration using extracellular flux analysis.
Optogenetic activation of renal sympathetic nerves significantly attenuated I/R-induced increases in serum creatinine and renal NGAL expression and reduced tubular injury. No alterations in systemic blood pressure or renal perfusion were observed, indicating that the renoprotective effect was independent of hemodynamic changes. scRNA-seq revealed prominent upregulation of mitochondrial respiratory chain genes, particularly NADH dehydrogenase (complex I) components, in proximal tubular cells following sympathetic stimulation. In HK-2 cells, norepinephrine suppressed hypoxia-induced NGAL expression, elevated the NAD⁺/NADH ratio, and increased mitochondrial proton leak, suggesting enhanced metabolic flexibility and reduced redox stress. Furthermore, renal tissues from stimulated mice exhibited decreased mitochondrial reactive oxygen species (ROS) accumulation compared with unstimulated controls.
Selective activation of renal sympathetic nerves protects against AKI by enhancing mitochondrial respiratory flexibility and reducing oxidative stress in tubular epithelial cells. This protection appears to involve partial uncoupling of oxidative phosphorylation, which limits ROS production while maintaining redox balance. These findings uncover a novel mitochondria-centered mechanism by which sympathetic nerve activity confers renal protection, highlighting a potential non-pharmacological strategy for AKI prevention and treatment through precise neuromodulation.
