ArticleProceedings of the National Academy of Sciences of the United States of America2020
Cell profiling of mouse acute kidney injury reveals conserved cellular responses to injury.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 422 papers.
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Who cites it
422 citing papers in PubMed.
- 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
- AMD1-mediated polyamine metabolism governs tubular repair fate by restraining senescence after kidney injury.Renal failure · 2026Article
- Triptolide in renal disorders: dual roles of therapeutic potential and nephrotoxicity: a narrative review.Pharmaceutical biology · 2026Review
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Epigenetically silencing gluconeogenic enzyme PCK1 by EZH2 promotes renal tubulointerstitial fibrosis.Molecular biomedicine · 2026Article
- Elevated glucose in kidney organoids induces tissue-intrinsic inflammation driving epithelial detachment.Stem cell reports · 2026Article
- Stress hyperglycemia ratio as a predictor of in-hospital mortality in patients with acute kidney injury: a retrospective cohort study.Clinical and experimental nephrology · 2026Article
- A cross-species single-cell kidney epigenome atlas reveals epithelial-dominant aging-like states in disease.Nature aging · 2026Article
- The role of senescence in kidney ageing, injury and fibrosis.Nature reviews. Nephrology · 2026Review
- SMOC2 promotes partial epithelial-mesenchymal transition and maladaptive repair in renal tubular epithelial cells.JCI insight · 2026Article
- HNF4A maintains proximal tubule identity and limits injury-associated cell states in the adult mouse kidney.bioRxiv : the preprint server for biology · 2026Article
- Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026Review
- SOCS2 Downregulation Is Associated with a Ferro-Aging-Related Transcriptomic Signature in Proximal Tubular Cells in Chronic Kidney Disease.Biomedicines · 2026Article
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- The GPX3-VCAM1 Axis Gates Pro-Fibrotic Tubule Cell Fate in Hyperuricemic Nephropathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Perilipin 2 drives cisplatin-induced acute kidney injury in young but not aged kidneys.American journal of physiology. Renal physiology · 2026Article
- Precision medicine in pediatric sepsis-associated acute kidney injury: when systemic heterogeneity meets organ-level heterogeneity.World journal of pediatrics : WJP · 2026Article
- A skin-kidney neutrophil axis links ultraviolet exposure to renal angiogenesis and tissue remodeling in healthy and lupus kidneys.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
362 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
After acute kidney injury (AKI), patients either recover or alternatively develop fibrosis and chronic kidney disease. Interactions between injured epithelia, stroma, and inflammatory cells determine whether kidneys repair or undergo fibrosis, but the molecular events that drive these processes are poorly understood. Here, we use single nucleus RNA sequencing of a mouse model of AKI to characterize cell states during repair from acute injury. We identify a distinct proinflammatory and profibrotic proximal tubule cell state that fails to repair. Deconvolution of bulk RNA-seq datasets indicates that this failed-repair proximal tubule cell (FR-PTC) state can be detected in other models of kidney injury, increasing during aging in rat kidney and over time in human kidney allografts. We also describe dynamic intercellular communication networks and discern transcriptional pathways driving successful vs. failed repair. Our study provides a detailed description of cellular responses after injury and suggests that the FR-PTC state may represent a therapeutic target to improve repair.
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