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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.
Renal tubular epithelial cells can convert external mechanical signals into intracellular chemical and electronic signals through mechanoreceptors. Piezo1 is a non-selective mechanosensitive cation channel that senses physical forces, inducing changes in membrane tension and opening to allow cation permeation. Recent studies indicate that Piezo1 is involved in the progression of chronic kidney disease, but its role in acute kidney injury (AKI) remains unclear.
We generated the renal proximal tubules (PT)-specific Piezo1 knockout mouse model and challenged with folic acid (FA) treatment and ischemia reperfusion (IR) operation to induce AKI, aiming to investigate the function of the mechanical-sensitive channel Piezo1 in AKI and its underlying mechanisms.
In vivo experiments revealed a significant increase in renal Piezo1 expression in folic acid (FA) or ischemia reperfusion (IR)-induced AKI mice models. PT-specific Piezo1 deletion attenuated acute kidney injury by inhibiting inflammatory cytokines infiltration and apoptosis. Moreover, knock-down of Piezo1 with small interfering RNA ameliorated the upregulation of kim-1 in H2O2 or hypoxia/reoxygenation (H/R)-treated HK-2 cells in vitro. RNA-seq data suggested that signal transducer and activator of transcription 1 (STAT1) may be a key downstream signaling by which Piezo1 is involved in the AKI process. Treatment of Piezo1 siRNA abolished the increased p-STAT1 abundance in H2O2 or H/R-treated HK-2 cells, while silence of STAT1 prevented the upregulation of kim-1, inflammatory cytokines, and apoptosis. Mechanistically, Piezo1 activation-induced p-STAT1 upregulation is at least partially linked to Ca2+-dependent CaMKII signaling. Co-IP experiments further demonstrated that Piezo1 agonist promotes the direct combination of CaMKII and STAT1.
This study uncovered the important role of Piezo1/CaMKII/STAT1 signaling in the development of acute kidney injury. Targeting the Piezo1 channels in renal proximal tubules may be a promising strategy for the treatment of AKI.
