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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.
Mammalian sterile twenty-like 1 (MST1), also known as Serine/threonine-protein kinase 4 (STK4), serves as a core component of the Hippo signaling pathway, which controls the organ size and cell numbers by modulating cell proliferation, differentiation and death. MST1 is abundantly expressed in the kidney. Our previous study revealed that renal tubule-specific Mst1 and Mst2 double knockout induced chronic kidney disease through mutual activation of the TNF-α and the Yap signaling pathways in mice. However, the specific role of tubular cell MST1 in kidney injury and fibrosis remains to be elucidated.
We generated renal tubule-specific Mst1 knockout (M1KO) mice by intercrossing floxed Mst1 mice with Ksp-Cre mice. Kidney injury was induced by unilateral ureteral obstruction (UUO) or intraperitoneal injection of cisplatin. Staurosporine (STS) was applied to trigger apoptosis in TKPTS mouse proximal tubular cells in vitro. We employed Masson’s trichrome staining, Picrosirius red staining, PAS staining and TUNEL assay to evaluate kidney injury and fibrosis after UUO or cisplatin. Moreover, qPCR, Western blotting, CCK-8 assay, immunoprecipitation, ATP assay, cell cycle assay and flow cytometry were used to determine the mechanisms responsible for the phenotypes observed.
MST1 protein expression in the kidney significantly increased in different kidney injury mouse models although the mRNA levels did not change. Compared with WT mice, M1KO mice exhibited increased tubular cell apoptosis and renal fibrosis following both UUO and cisplatin treatment, and these effects were independent of YAP. Inhibition of MST1 expression enhanced cell apoptosis induced by serum starvation or by STS in TKPTS cells, HK2 cells and primary tubular epithelial cells (PTECs), without any effects on the YAP activity. Moreover, under hypoxic conditions, MST1 depletion regulated ATP levels in TKPTS and promoted Caspase cleavage in TKPTS cells and PTECs independently of YAP signaling, accompanied by a specific upregulation of FoxO1 and FoxO3 that was not triggered by starvation. Conversely, MST1 overexpression inhibited apoptosis dose-dependently in TKPTS cells.
MST1 deficiency significantly exacerbates kidney injury and fibrosis independently of YAP. Increased MST1 expression in response to kidney injury protects against tubular cell death.
The content presented in this abstract was submitted for the 23rd Asian Pacific Congress of Nephrology.
