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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.
Hemodynamic factors such as glomerular hypertension and hyperfiltration are major contributors to glomerular injury. However, the molecular mechanisms by which glomerular cells sense and respond to mechanical forces remain poorly understood. Piezo1, a mechanosensitive ion channel, regulates diverse physiological and pathological processes, including hypertension and hypertensive nephropathy. Here, we investigated the role of Piezo1 in podocytes under basal and pressure-loaded conditions using genetically modified mice and cultured podocytes.
Podocyte-specific Piezo1 knockout mice (pPiezo1 KO) and littermate controls (pPiezo1 WT) were generated by crossing Nphs1Cre/+ mice with Piezo1flox/flox mice. Hypertensive nephropathy was induced by short-term salt-loaded angiotensin II infusion (AII/HS, 2 weeks) and long-term salt-loaded aldosterone infusion with uninephrectomy (UNx/Ald/HS, 6 weeks). RNA-sequencing was performed on glomeruli from pPiezo1 WT and KO mice, as well as cultured podocytes treated with or without the Piezo1 activator Yoda1.
Under basal conditions, pPiezo1 WT and KO mice showed no differences in blood pressure, albuminuria, renal histology, or podocyte ultrastructure. Following AII/HS, both groups developed comparable hypertension; however, pPiezo1 KO mice exhibited significantly greater albuminuria, podocyte injury, and glomerulosclerosis. Similar findings were observed in the chronic UNx/Ald/HS model. Transcriptome analysis of glomeruli revealed altered expression of several genes, including Rhpn1 and Fgfbp1. In cultured podocytes, Yoda1 stimulation induced distinct transcriptional changes, including Pai1, Sgk1, and Mcp1. Podocyte injury in AII/HS-treated pPiezo1 KO mice was prevented by losartan and hydralazine, and partially ameliorated by the Rho kinase inhibitor fasudil.
Piezo1 is dispensable for podocyte maintenance under basal conditions but is essential for adaptation to mechanical stress. Its absence leads to severe podocyte injury, albuminuria, and glomerulosclerosis under both short- and long-term hypertensive stress. These findings highlight Piezo1 as a key mechanosensor in podocytes, with both insufficient and excessive activity potentially driving injury through distinct signaling pathways.
