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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.
We previously reported that p38 mitogen-activated protein kinase (MAPK) contributes to podocyte injury by aldosterone. However, since aldosterone exerts systemic effects, the precise role of p38 MAPK in podocyte injury remains unclear. This study aimed to elucidate the specific role of podocyte p38 MAPK using both in vivo and in vitro, particularly its involvement in autophagy regulation via ULK1 phosphorylation.
To investigate the role of p38 MAPK in podocyte injury, we crossed NEP25 mice, which develop podocyte-specific injury, with podocyte-specific p38 MAPK knockout mice (cKO). Podocyte injury was induced by immunotoxin administration, and proteinuria, histological changes, and RNA sequencing were evaluated. For in vitro experiments, cultured human podocytes with p38 MAPK knockout via CRISPR/Cas9 were exposed to adriamycin, and autophagy-related pathways were assessed by Western blot, focusing on autophagic flux and ULK1 phosphorylation status.
Following immunotoxin-induced podocyte injury, proteinuria peaked at week 2 in control mice, whereas cKO mice exhibited significantly increased proteinuria at both weeks 1 and 2. Histological examination revealed significantly worse segmental sclerosis, crescent formation, and podocyte foot process effacement in cKO mice. Immunofluorescence staining of glomeruli demonstrated increased expression of cleaved caspase-3, p62, and LAMP1, suggesting the involvement of apoptosis and autophagy. RNA sequencing with cell-type deconvolution showed increased expression of ATG7 and LC3 with decreased GABARAPL1 in cKO mice. Gene Ontology (GO) analysis indicated impaired cellular catabolic function and energy metabolism pathways. In vitro experiments using adriamycin-injured cultured human podocytes demonstrated that p38 MAPK knockout resulted in reduced autophagic flux and decreased phosphorylation of ULK1 at Ser757.
Podocyte-specific p38 MAPK deletion exacerbated kidney injury in the FSGS model. Our findings suggest that p38 MAPK deficiency inhibits ULK1 phosphorylation, leading to autophagic dysfunction accompanied by energy metabolic disturbances, ultimately resulting in the worsened podocyte injury. These results highlight that p38 MAPK in podocytes plays a crucial role in maintaining podocyte homeostasis through the regulation of autophagy via ULK1 mediated-signaling.
