ArticleNature communications2025
Controlling nephron precursor differentiation to generate proximal-biased kidney organoids with emerging maturity.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Review
- ChEA-KG and ChEA-KG-TS: a network-based transcription factor enrichment analysis tool with an accompanying time-series workflow.Nucleic acids research · 2026Article
- Redox control at the ER-mitochondria interface in kidney transplantation: MAM-centered stress signaling and translational organoid platforms.Redox biology · 2026Review
- Organoids: generation strategies, applications, and future challenges.Stem cell research & therapy · 2026Review
- Developmentally inspired synthetic kidney engineering.Nature biotechnology · 2026Review
- Kidney Organoids in Drug Development: Integrating Technological Advances and Standardization for Effective Implementation.Advanced healthcare materials · 2026Review
- Parsing Glomerular and Tubular Structure Variability in High-Throughput Kidney Organoid Culture.Methods and protocols · 2025Article
- Axial nephron fate switching demonstrates a plastic system tunable on demand.Nature communications · 2025Article
- Mathematical modeling reveals cell differentiation processes and progenitor kinetics necessary for proper nephrogenesis.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
The kidney maintains fluid homeostasis by reabsorbing essential compounds and excreting waste. Proximal tubule cells, crucial for reabsorbing sugars, ions, and amino acids, are highly susceptible to injury, often leading to pathologies necessitating dialysis or transplants. Human pluripotent stem cell-derived kidney organoids offer a platform to model renal development, function, and disease, but proximal nephron differentiation and maturation in these structures is incomplete. Here, we drive proximal tubule development in pluripotent stem cell-derived kidney organoids by mimicking in vivo proximal differentiation. Transient PI3K inhibition during early nephrogenesis activates Notch signaling, shifting nephron axial differentiation towards epithelial and proximal precursor states that mature to proximal convoluted tubule cells broadly expressing physiology-imparting solute carriers including organic cation and organic anion family members. The "proximal-biased" organoids thus acquire function, and on exposure to nephrotoxic injury, display tubular collapse and DNA damage, and upregulate injury response markers HAVCR1/KIM1 and SOX9 while downregulating proximal transcription factor HNF4A. Here, we show that proximally biased human-derived kidney organoids provide a robust model to study nephron development, injury responses, and a platform for therapeutic discovery.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.