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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.
Glomerular podocyte injury is characteristic in the development and progression of diabetic nephropathy (DN). However, the targeted therapies are currently lacking. The expression and function of lactase-like protein (LCTL), a type-I single-pass transmembrane protein also known as γ-Klotho, in DN was not previously explored.
LCTL expression was assessed in kidney biopsies and serum from DN patients and in streptozotocin-induced diabetic mice. Functional roles were evaluated using LCTL knockout, CLIC5 knockout mice, and LCTL overexpression via lentiviral vectors. Cultured podocytes were used to examine the effects of LCTL on CLIC5A expression. Rac1 activation and PI4P5 kinase interactions were assessed by PAK-PBD pulldown.
We observed two LCTL isoforms: a circulating soluble, and a membrane-bound isoform, the latter predominantly expressed in podocytes. In DN patients and in mice with streptozotocin-induced diabetes, circulating and podocyte LCTL abundance were reduced, and the reduction in LCTL levels strongly correlated with the loss of renal function in diabetic nephropathy. LCTL deletion in mice markedly exacerbated diabetes-induced glomerular injury, and in NOS3 deficient diabetic mice glomerular injury was partially reversed by LCTL overexpression. LCTL deficiency in mice depressed glomerular CLIC5A expression, and in cultured podocytes LCTL silencing reduced, and LCTL overexpression stimulated CLIC5A expression. LCTL and CLIC5A co-localized at the podocyte plasma membrane and co-immuno-precipitated from cell lysates. Overexpression of membrane-spanning LCTL in podocytes promoted ezrin phosphorylation and actin polymerization, mimicking CLIC5A effects. CLIC5A stimulated the association of PI4P5 kinases with Rac1-GTP and in mouse kidneys, the association of the PI4P5Kα3 isoform with Rac1-GTP was selectively CLIC5A-dependent. In diabetic mice glomerular CLIC5A abundance decreased, and CLIC5A deletion mimicked the effects of LCTL deletion.
The membrane-spanning LCTL isoform, acting at least partly via CLIC5A, plays a critical protective role against diabetes-induced podocyte injury and is a potential therapeutic target in DN progression.
