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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.
GLP-1 analogs have been demonstrated to exert protective effects in various organ fibrosis models, including renal fibrosis. However, the underlying mechanisms by which they ameliorate the progression of chronic kidney disease (CKD) remain unclear. This study aims to investigate whether GLP-1 can effectively attenuate renal fibrosis in mice with folic acid-induced nephropathy, and whether this protective effect is mediated through the regulation of T cell differentiation, particularly the balance between Th cells and Treg cells.
A CD4+ T cell-specific GLP-1R knockout mouse model (CD4-GLP-1R cKO, cKO) was generated. Renal fibrosis was induced in these mice and their wild-type (WT) littermates by a single intraperitoneal injection of folic acid (FA, 250 mg/kg). Mice were randomly assigned to four groups: cKO-FA, WT-FA, and corresponding vehicle-control groups for both genotypes. Renal function, histology, inflammatory cytokine levels, and fibrosis markers were assessed four weeks post-injection.
Conditional knockout of GLP1-R in CD4+ T cells markedly exacerbated FA-induced renal dysfunction and inflammatory tissue injury in mice. Compared with the WT-FA group, the cKO-FA group exhibited significantly higher levels of BUN and SCr, indicating impaired renal function. Additionally, histopathological assessments revealed more severe tubular atrophy, inflammatory cell infiltration, and renal interstitial fibrosis in the cKO-FA group, along with significantly increased expression of Col1α1 and α-SMA. Mechanistically, the expression of lineage-specific transcription factors RORγt (for Th17) and T-bet (for Th1) was significantly upregulated in renal tissue, whereas the expression of Foxp3, a marker of Tregs, was downregulated. Concurrently, levels of pro-inflammatory cytokines (IL-6, TNF-α, and IFN-γ) were elevated, while the anti-inflammatory cytokine IL-10 was markedly reduced. These findings suggest that GLP-1 may modulate T cell differentiation and disrupt the balance between Ths and Tregs.
GLP-1 effectively prevents the progression from AKI to CKD and renal fibrosis, an effect that is at least partially mediated by modulating CD4+ T cell differentiation to maintain the balance of Th/Treg. Therefore, GLP-1 analog is a promising therapeutic agent that may halt the progression of renal fibrosis.
