located near both the vascular and urinary poles adjacent to podocyte. This suggests that Cdkn1a PECs may act as progenitor cells capable of partially compensating for podocyte function or transitioning into podocyte. Pseudotime trajectory and interaction analyses further found Jag1-Notch2 signaling as a key mediator of PEC-to-podocyte conversion. Stimulation with Jag1 promoted podocyte redifferentiation, indicating that activation of the Notch2 pathway is a crucial mechanism in this transition. Furthermore, transcriptomic profiling showed that inhibition of lysine demethylase 1A (KDM1A) with GSK 2879552 upregulates histone H3 lysine 4 mono-/dimethylation (H3K4me1/2), leading to reactivation of Notch2 target genes and restoration of podocyte numbers. Conclusion: Collectively, these findings provide novel mechanistic insights and highlight potential therapeutic targets for podocyte repair and regeneration in DKD. I have no potential conflict of interest to disclose. I did not use generative AI and AI-assisted technologies in the writing process.
Chen et al. (Wed,) studied this question.
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