ArticleStem cell research & therapy2024
KCNJ16-depleted kidney organoids recapitulate tubulopathy and lipid recovery upon statins treatment.
Article in Stem cell research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- CRISPR screening redefines therapeutic target identification and drug discovery with precision and scalability.Journal of pharmaceutical analysis · 2026Review
- Advances and future perspectives of kidney organoid technology in renal disease research and clinical translation.Frontiers in medicine · 2026Review
- Modeling kidney fibrosis and tubular regeneration in iPSC-derived kidney organoids.Stem cell research & therapy · 2025Article
- Immune and Immune-Integrated Organoids as NextGeneration Platforms for Disease Modeling.MedComm · 2025Review
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8 authors.
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Abstract
backgroundThe KCNJ16 gene has been associated with a novel kidney tubulopathy phenotype, viz. disturbed acid-base homeostasis, hypokalemia and altered renal salt transport. KCNJ16 encodes for Kir5.1, which together with Kir4.1 constitutes a potassium channel located at kidney tubular cell basolateral membranes. Preclinical studies provided mechanistic links between Kir5.1 and tubulopathy, however, the disease pathology remains poorly understood. Here, we aimed at generating and characterizing a novel advanced in vitro human kidney model that recapitulates the disease phenotype to investigate further the pathophysiological mechanisms underlying the tubulopathy and potential therapeutic interventions.
methodsWe used CRISPR/Cas9 to generate KCNJ16 mutant (KCNJ16
resultsKCNJ16-depleted kidney organoids showed transcriptomic and potential functional impairment of key voltage-dependent electrolyte and water-balance transporters. We observed cysts formation, lipid droplet accumulation and fibrosis upon Kir5.1 function loss. Furthermore, a large scale, glutamine tracer flux metabolomics analysis demonstrated that KCNJ16
conclusionsMature kidney organoids represent a relevant in vitro model for investigating the function of Kir5.1. We discovered novel molecular targets for this genetic tubulopathy and identified statins as a potential therapeutic strategy for KCNJ16 defects in the kidney.
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