ArticleNature communications2023
RAAS-deficient organoids indicate delayed angiogenesis as a possible cause for autosomal recessive renal tubular dysgenesis.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Kidney organoids as models for hereditary kidney diseases: Toward precision medicine (Review).Experimental and therapeutic medicine · 2026Review
- Single-cell transcriptomic comparison of tubular segment maturation in advanced humaniScience · 2026Article
- Single-cell sequencing and organoids: applications in organ development and disease.Molecular biomedicine · 2025Review
- Organoids in Genetic Disorders: from Disease Modeling to Translational Applications.Stem cell reviews and reports · 2025Review
- Integrating collecting systems in human kidney organoids through fusion of distal nephron to ureteric bud.Cell stem cell · 2025Article
- Organoids-on-Chips Technology: Unveiling New Perspectives in Rare-Disease Research.International journal of molecular sciences · 2025Review
- Biomedical applications of organoids in genetic diseases.Medical review (2021) · 2025Review
- Reprogramming of iPSCs to NPCEC-like cells by biomimetic scaffolds for zonular fiber reconstruction.Bioactive materials · 2025Article
- Spatially defined microenvironment for engineering organoids.Biophysics reviews · 2024Review
- Scalable production of uniform and mature organoids in a 3D geometrically-engineered permeable membrane.Nature communications · 2024Article
- Kidney organoids: steps towards better organization and function.Biochemical Society transactions · 2024Review
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Autosomal Recessive Renal Tubular Dysgenesis (AR-RTD) is a fatal genetic disorder characterized by complete absence or severe depletion of proximal tubules (PT) in patients harboring pathogenic variants in genes involved in the Renin-Angiotensin-Aldosterone System. To uncover the pathomechanism of AR-RTD, differentiation of ACE-/- and AGTR1-/- induced pluripotent stem cells (iPSCs) and AR-RTD patient-derived iPSCs into kidney organoids is leveraged. Comprehensive marker analyses show that both mutant and control organoids generate indistinguishable PT in vitro under normoxic (21% O2) or hypoxic (2% O2) conditions. Fully differentiated (d24) AGTR1-/- and control organoids transplanted under the kidney capsule of immunodeficient mice engraft and mature well, as do renal vesicle stage (d14) control organoids. By contrast, d14 AGTR1-/- organoids fail to engraft due to insufficient pro-angiogenic VEGF-A expression. Notably, growth under hypoxic conditions induces VEGF-A expression and rescues engraftment of AGTR1-/- organoids at d14, as does ectopic expression of VEGF-A. We propose that PT dysgenesis in AR-RTD is primarily a non-autonomous consequence of delayed angiogenesis, starving PT at a critical time in their development.
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Registered trials
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