ArticleNature communications2022
Tubular cell polyploidy protects from lethal acute kidney injury but promotes consequent chronic kidney disease.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 68 citations in OpenAlex.
- Insights from integrative spatial transcriptomics in sepsis-associated acute kidney injury.Nature reviews. Nephrology · 2026Review
- Targeting the lncRNA PVT-1-Hippo signaling axis in kidney diseases: an emerging therapeutic paradigm.Molecular biology reports · 2026Review
- Targeting YAP1-Mediated Tubular Cell Senescence to Attenuate Maladaptive Repair and Fibrotic Transition After Acute Kidney Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- SGLT2i, anti-endothelin A and double endothelin and angiotensin inhibitors: a new future for chronic kidney disease in children.Pediatric nephrology (Berlin, Germany) · 2026Review
- Single-cell RNA sequencing and spatial transcriptomics in the discovery of kidney disease potential biomarkers: a narrative review.BMC nephrology · 2026Review
- Growth under pressure: The pros and cons of polyploidy induced by stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Review
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Multifactorial chronic kidney disease and the kidney capacity-workload balance.Nature reviews. Nephrology · 2026Review
- Acute kidney injury over the past decade: from definition evolution to pathogenesis insights and innovative therapeutic strategies.Cellular and molecular life sciences : CMLS · 2026Review
- Matricellular protein SMOC2 safeguards tubular integrity in acute kidney injury via integrin β3-dependent inhibition of CCND1-CDK4/6 axis.Molecular biomedicine · 2026Article
- Distinct p21 dynamics drive alternative routes to whole-genome duplication through a common CDK4/6-dependent polyploid G0 state.bioRxiv : the preprint server for biology · 2026Article
- Reappraisal of profibrotic phenotype and cell-cycle state of renal tubular epithelium after ischemia-reperfusion injury.PloS one · 2026Article
- Cell Fusion-Mediated Induction of Polyploidy, Aneuploidy, and Genomic Instability in Cancer Cells.Advances in experimental medicine and biology · 2026Review
- Life history enlightened therapies: cell cycle mapping to identify molecular targets to prevent hepatocellular carcinoma.Evolution, medicine, and public health · 2026Article
- Activation of a Src-JNK pathway in unscheduled endocycling cells of the Drosophila wing disc induces a chronic wounding response.Genetics · 2025Article
- Progress and applications of single-cell RNA sequencing and spatial transcriptome technology in acute kidney injury research.Molecular therapy. Nucleic acids · 2025Review
- Melanization regulates wound healing by limiting polyploid cell growth in the Drosophila epithelium.Genetics · 2025Article
- NSD1-916aa encoded by CircNSD1 contributes to AKI-to-CKD transition through inducing ferroptosis in tubular epithelial cells.JCI insight · 2025Article
- Noncanonical function of Pannexin1 promotes cellular senescence and renal fibrosis post-acute kidney injury.Nature communications · 2025Article
- Understanding and targeting senescence in kidney disease.Clinical kidney journal · 2025Review
Corrections and comments
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Authors and funding
27 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is frequent, often fatal and, for lack of specific therapies, can leave survivors with chronic kidney disease (CKD). We characterize the distribution of tubular cells (TC) undergoing polyploidy along AKI by DNA content analysis and single cell RNA-sequencing. Furthermore, we study the functional roles of polyploidization using transgenic models and drug interventions. We identify YAP1-driven TC polyploidization outside the site of injury as a rapid way to sustain residual kidney function early during AKI. This survival mechanism comes at the cost of senescence of polyploid TC promoting interstitial fibrosis and CKD in AKI survivors. However, targeting TC polyploidization after the early AKI phase can prevent AKI-CKD transition without influencing AKI lethality. Senolytic treatment prevents CKD by blocking repeated TC polyploidization cycles. These results revise the current pathophysiological concept of how the kidney responds to acute injury and identify a novel druggable target to improve prognosis in AKI survivors.
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