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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.
The main pathological hallmark of kidney disease progression is renal tubulointerstitial fibrosis, the final common pathway leading to renal failure, yet effective therapies remain limited. Semaphorin 3A (SEMA3A), a secreted and membrane-associated protein, regulates immune responses, cell survival, migration, and angiogenesis. In adult kidneys, SEMA3A is expressed in tubular epithelial cells and podocytes, and excessive activation of SEMA3A signaling via its receptor neuropilin-1 (NRP1) exacerbates renal injury. Our previous work revealed that SEMA3A promotes fibrosis by inducing epithelial–mesenchymal transition (EMT) in tubular cells and enhancing extracellular matrix production in fibroblasts via c-Jun N-terminal kinase (JNK) signaling. This study aimed to assess the antifibrotic efficacy of a neutralizing anti-SEMA3A monoclonal antibody (BMAA) in murine models of renal fibrosis.
Two mouse models of renal fibrosis were established: unilateral ureteral obstruction (UUO) and aristolochic acid I (AA)-induced nephropathy in 8-week-old wild-type male mice. Mice were administered vehicle or BMAA (100 µg or 500 µg, intravenously) and sacrificed on day 7 (UUO) or day 30 (AA). Renal injury and fibrosis were assessed using H&E, Masson’s trichrome (MT), immunofluorescence (IF), and Western blotting (WB). The expression of NRP1, fibronectin, E-cadherin, and vimentin was evaluated. In vitro, human renal tubular epithelial (HK-2) cells were stimulated with TGF-β1 in the presence or absence of BMAA to examine its effects on EMT and ECM production.
In both UUO and AA models, NRP1 expression was markedly increased in proximal tubular cells and interstitial myofibroblasts. Treatment with BMAA significantly attenuated renal fibrosis, as evidenced by reduced collagen deposition on MT staining and α-SMA, and decreased expression of fibronectin on WB and IF. IF revealed vimentin-positive proximal tubular cells, indicative of EMT, in vehicle-treated kidneys, whereas these cells were markedly reduced in the BMAA-treated groups. Consistently, the E-cadherin/vimentin ratio was significantly decreased in both fibrosis models but was restored by BMAA treatment. In vitro, BMAA suppressed TGF-β1–induced EMT in HK-2 cells by preserving E-cadherin/vimentin ratio. These findings suggest that BMAA inhibits SEMA3A signaling, thereby suppressing tubular EMT and consequently attenuating renal fibrosis.
Our findings demonstrate that SEMA3A signaling plays a pivotal role in the development of renal fibrosis by promoting EMT in tubular epithelial cells and activating interstitial myofibroblasts. The neutralizing anti-SEMA3A antibody BMAA effectively suppressed fibrosis in two distinct experimental models, indicating dual protective effects on tubular and stromal compartments. These results highlight SEMA3A as a novel profibrotic mediator and suggest that antibody-based inhibition of SEMA3A signaling may represent an innovative therapeutic approach for preventing renal fibrosis and delaying CKD progression.
