ArticleEMBO molecular medicine2025
Loss of p300 in proximal tubular cells reduces renal fibrosis and endothelial-mesenchymal transition.
Article in EMBO molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Deficiency of GCN5 exacerbates pulmonary fibrosis by disrupting the LKB1-AMPK pathway.Cell communication and signaling : CCS · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Lactylation in kidney diseases: a review of regulatory mechanisms and therapeutic prospects.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
10 authors.
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Abstract
Chronic kidney disease (CKD) has a high prevalence worldwide and is typically accompanied by severe fibrosis. However, the exact pathogenesis of renal fibrosis and effective treatments have yet to be identified. In this study, we found that expression of the histone-acetyltransferase p300 was increased in focal segmental glomerulosclerosis patients and several distinct mouse models of renal fibrosis. Moreover, we showed that the AKT-mediated phosphorylation of Ser-1834 of p300 increased the stability of p300 upon renal fibrosis induction, and conversely, PPM1K specifically dephosphorylated p300 at Ser-1834, resulting in a significant reduction in p300 stability and renal fibrosis. Interestingly, increased p300 in proximal tubular cells (PTCs) promoted renal fibrosis development by mediating the endothelial to mesenchymal transition (EndMT) via upregulation of the mesenchymal-transition-related secreted proteins POSTN, FSTL1, and FSCN1. Both EndMT and renal fibrosis were significantly diminished by either PTC-specific deletion of p300 gene or selective inhibitors of p300. Collectively, our results demonstrate the role of p300 in the development of renal fibrosis, and suggest that p300 is a promising target for treatment of advanced CKD.
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