ArticleGenome medicine2022
Single-cell transcriptomics reveals common epithelial response patterns in human acute kidney injury.
Article in Genome medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 105 citations in OpenAlex.
- Effect of felzartamab on the molecular phenotype of antibody-mediated rejection in kidney transplant biopsies.Nature medicine · 2025Trial
- A four-gene signature for diagnosis of acute kidney injury following kidney transplantation.Renal failure · 2026Article
- Kidney Transcriptome Sequencing Improves Molecular Diagnosis and Reveals Splicing Complexity Across the Alport Spectrum.Kidney international reports · 2026Article
- Spatial Transcriptomics and Mechanisms of Immune Checkpoint Inhibitor-Associated Interstitial Nephritis.Kidney international reports · 2026Article
- Review
- Synchronization of the 12-h circatidal rhythm maintains the kidney through repeated cycles of warm reperfusion in the hibernating ground squirrel.Function (Oxford, England) · 2026Article
- Insights from integrative spatial transcriptomics in sepsis-associated acute kidney injury.Nature reviews. Nephrology · 2026Review
- Caveolin-1 Stabilizes SERCA2 to Counteract Acute Kidney Injury via Suppression of CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Impact of older donor age in kidney transplants in a biopsy-based observational study.JCI insight · 2026Observational
- Single-cell transcriptomic comparison of tubular segment maturation in advanced humaniScience · 2026Article
- Inhibition of (interstitial) P2YPflugers Archiv : European journal of physiology · 2026Article
- Article
- Endothelial prolyl hydroxylase 3 mitigates maladaptive inflammation to promote post-ischemic kidney repair.Kidney international · 2026Article
- Association between HALP score and in-hospital outcomes in patients with acute kidney injury: a retrospective cohort study.Scientific reports · 2026Article
- HMGB1-mediated formation of IL-33-abundant NETs drives lung-to-kidney injury in severe pneumonia-associated acute kidney injury.JCI insight · 2026Article
- Article
- Deletion of exocyst component 5 suppresses repair of injured kidney by limiting cell proliferation.Cell death discovery · 2026Article
- Integrative Network Pharmacology and Molecular Docking Analysis Uncovers Multi-Target Mechanisms of Alpha-Mangostin Against Acute Kidney Injury.Foods (Basel, Switzerland) · 2026Article
- Identification and functional validation of mitochondria-related genes associated with tubular injury in kidney transplantation and ischemia-reperfusion injury.Biology direct · 2026Article
- Inhibition of (interstitial) P2YResearch square · 2026Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
26 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute kidney injury (AKI) occurs frequently in critically ill patients and is associated with adverse outcomes. Cellular mechanisms underlying AKI and kidney cell responses to injury remain incompletely understood.
methodsWe performed single-nuclei transcriptomics, bulk transcriptomics, molecular imaging studies, and conventional histology on kidney tissues from 8 individuals with severe AKI (stage 2 or 3 according to Kidney Disease: Improving Global Outcomes (KDIGO) criteria). Specimens were obtained within 1-2 h after individuals had succumbed to critical illness associated with respiratory infections, with 4 of 8 individuals diagnosed with COVID-19. Control kidney tissues were obtained post-mortem or after nephrectomy from individuals without AKI.
resultsHigh-depth single cell-resolved gene expression data of human kidneys affected by AKI revealed enrichment of novel injury-associated cell states within the major cell types of the tubular epithelium, in particular in proximal tubules, thick ascending limbs, and distal convoluted tubules. Four distinct, hierarchically interconnected injured cell states were distinguishable and characterized by transcriptome patterns associated with oxidative stress, hypoxia, interferon response, and epithelial-to-mesenchymal transition, respectively. Transcriptome differences between individuals with AKI were driven primarily by the cell type-specific abundance of these four injury subtypes rather than by private molecular responses. AKI-associated changes in gene expression between individuals with and without COVID-19 were similar.
conclusionsThe study provides an extensive resource of the cell type-specific transcriptomic responses associated with critical illness-associated AKI in humans, highlighting recurrent disease-associated signatures and inter-individual heterogeneity. Personalized molecular disease assessment in human AKI may foster the development of tailored therapies.
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