ArticleStem cell research & therapy2022
Modeling oxidative injury response in human kidney organoids.
Article in Stem cell research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 29 citations in OpenAlex.
- Modelling ischaemic AKI in human kidney organoids reveals injury-associated epithelial states and macrophage-epithelial crosstalk.Genome medicine · 2026Article
- Redox control at the ER-mitochondria interface in kidney transplantation: MAM-centered stress signaling and translational organoid platforms.Redox biology · 2026Review
- Article
- Induction of fibrosis in human kidney organoids delineates mechanisms and therapeutic targets of fibrotic kidney disease.Stem cell research & therapy · 2026Article
- Serum HDAC3 as an early biomarker for prediction and staging of sepsis-associated AKI: prospective cohort study.BMC infectious diseases · 2026Article
- Kidney Organoids in Drug Development: Integrating Technological Advances and Standardization for Effective Implementation.Advanced healthcare materials · 2026Review
- Protecting kidney function: from mechanisms to therapeutic targets and traditional Chinese medicine.Renal failure · 2025Review
- Kidney Fibrosis In Vitro and In Vivo Models: Path Toward Physiologically Relevant Humanized Models.Advanced healthcare materials · 2025Review
- A genetically inducible endothelial niche enables vascularization of human kidney organoids with multilineage maturation and emergence of renin expressing cells.Kidney international · 2024Article
- Podocyte injury at young age causes premature senescence and worsens glomerular aging.American journal of physiology. Renal physiology · 2024Article
- Navigating the kidney organoid: insights into assessment and enhancement of nephron function.American journal of physiology. Renal physiology · 2023Review
- Ascorbate protects human kidney organoids from damage induced by cell-free hemoglobin.Disease models & mechanisms · 2023Article
- In-silico and in-vitro morphometric analysis of intestinal organoids.PLoS computational biology · 2023Article
- Article
- Genetically engineering endothelial niche in human kidney organoids enables multilineage maturation, vascularization and de novo cell types.bioRxiv : the preprint server for biology · 2023Article
- Large-Scale Production of Kidney Organoids from Human Pluripotent Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Functional characterization of ion channels expressed in kidney organoids derived from human induced pluripotent stem cells.American journal of physiology. Renal physiology · 2022Article
- Disease Modeling with Kidney Organoids.Micromachines · 2022Review
- Physiology assays in human kidney organoids.American journal of physiology. Renal physiology · 2022Review
- Identifying Common Molecular Mechanisms in Experimental and Human Acute Kidney Injury.Seminars in nephrology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundHemolysis occurs in many injury settings and can trigger disease processes. In the kidney, extracellular hemoglobin can induce damage via several mechanisms. These include oxidative stress, mitochondrial dysfunction, and inflammation, which promote fibrosis and chronic kidney disease. Understanding the pathophysiology of these injury pathways offers opportunities to develop new therapeutic strategies.
methodsTo model hemolysis-induced kidney injury, human kidney organoids were treated with hemin, an iron-containing porphyrin, that generates reactive oxygen species. In addition, we developed an induced pluripotent stem cell line expressing the biosensor, CytochromeC-GFP (CytoC-GFP), which provides a real-time readout of mitochondrial morphology, health, and early apoptotic events.
resultsWe found that hemin-treated kidney organoids show oxidative damage, increased expression of injury markers, impaired functionality of organic anion and cation transport and undergo fibrosis. Injury could be detected in live CytoC-GFP organoids by cytoplasmic localization of fluorescence. Finally, we show that 4-(phenylthio)butanoic acid, an HDAC inhibitor with anti-fibrotic effects in vivo, reduces hemin-induced human kidney organoid fibrosis.
conclusionThis work establishes a hemin-induced model of kidney organoid injury. This platform provides a new tool to study the injury and repair response pathways in human kidney tissue and will assist in the development of new therapeutics.
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.