ArticleBiology direct2026
JUNB transcriptional regulation of KRT20 via ITGB1 activates PI3K/AKT signaling pathway against fibrosis-induced by renal injury.
Article in Biology direct, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Chronic kidney disease and its progression to end-stage renal disease represent a major global health burden, driven by renal interstitial fibrosis. The function of the intermediate filament protein Keratin 20 (KRT20) in this context remains largely unexplored. This study investigated the role and mechanism of KRT20 in renal fibrosis. Integrated transcriptomic analysis revealed significant upregulation of KRT20 in fibrotic kidneys. With unilateral ureteral obstruction (UUO) mouse models and TGF-β1-stimulated human renal tubular epithelial (HK-2) cells, we found that KRT20 expression increased progressively with fibrotic severity. Functional studies demonstrated that KRT20 knockdown exacerbated fibrosis and epithelial-mesenchymal transition while its overexpression attenuated. Mechanistically, the transcription factor JUNB, activated by TGF-β1, directly bound to the KRT20 promoter to drive its transcription. Upregulated KRT20 protein subsequently interacted with integrin ITGB1, leading to activation of the PI3K/AKT survival signaling pathway. Collectively, these findings delineated a novel protective “JUNB–KRT20–ITGB1–PI3K/AKT” axis in renal fibrosis, identifying KRT20 as a potential therapeutic target for enhancing endogenous anti-fibrotic response.
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