ArticleStem cell research & therapy2025
Modeling kidney fibrosis and tubular regeneration in iPSC-derived kidney organoids.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Mitochondrial dysfunction of renal tubular epithelial cells in chronic kidney disease-associated fibrosis: from organelle homeostasis to multicellular remodeling.Molecular biology reports · 2026Review
- Bridging Kidney Organoid Innovation and Regenerative Medicine: Current Advances and Future Directions.Cell proliferation · 2026Review
- Therapeutic Applications of Induced Pluripotent Stem Cell Technology in Kidney Disease: A Systematic Review and Meta-Analysis.Kidney diseases (Basel, Switzerland)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundKidney fibrosis is one of the pathological hallmarks of chronic kidney disease, likely contributing to the loss of kidney function. The mechanisms leading to kidney fibrosis and its reversibility is only partially understood, which hampers the development of therapeutic targets. Therefore, it is crucial to establish a robust human in vitro model that can be used to study kidney fibrosis and potential regeneration.
methodsHuman induced pluripotent stem cells (iPSC) were differentiated into kidney organoids. Fibrotic injury was induced by mimicking hypoxia (1% O
resultsThe combination of hypoxia and IL-1β induced the strongest fibrotic response with significant upregulation of FN1 and collagen type I, and loss of tubular and glomerular markers. Over time, FN1 levels realigned with the control group, whereas collagen type I remained elevated. Tubular markers (Villin and ECAD) recovered to near-control levels, coinciding with increased CD133+ and CD24+ cell population and Ki67 expression. In contrast, PODXL+ glomerular structures showed limited recovery.
conclusionsWe present a reproducible human kidney organoid model that captures both fibrotic remodeling and tubular regeneration following clinically relevant injury. This platform offers a valuable tool for studying kidney-specific fibrosis dynamics and testing anti-fibrotic or pro-regenerative strategies.
Indexed as
Identifiers
What OpenQuestion holds
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.