ArticleNature communications2022
Defining cellular complexity in human autosomal dominant polycystic kidney disease by multimodal single cell analysis.
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 77 papers.
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Who cites it
77 citing papers in PubMed, 99 citations in OpenAlex.
- Novel Roles of GPCRs in the Renal Collecting Duct.Physiology (Bethesda, Md.) · 2026Review
- Pirfenidone treatment attenuates fibrosis in autosomal dominant polycystic kidney disease.JCI insight · 2026Article
- Cilia-to-basement membrane signaling is a biomechanical driver in models of autosomal dominant polycystic kidney disease.The Journal of clinical investigation · 2026Article
- Evidence for a tubular basement membrane-cilia connection in autosomal dominant polycystic kidney disease pathogenesis.The Journal of clinical investigation · 2026Article
- A cross-model single-cell atlas reveals conserved involvement of osteopontin in polycystic kidney disease.JCI insight · 2026Article
- Kidney-specific deletion of the BicC family RNA-binding protein 1 triggers an ADPKD-like cystogenic program.iScience · 2026Article
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Matrix Gla Protein is a novel regulator of TGFβ-dependent fibroblast activation and kidney fibrosis.Molecular biomedicine · 2026Article
- Combination siRNA delivery as a therapeutic strategy for ADPKD.bioRxiv : the preprint server for biology · 2026Article
- Species, cell proliferation state and oxygen partial pressure are major factors in the in vitro toxicity of repurposed potential ADPKD drugs in human and murine renal proximal tubule cells.Archives of toxicology · 2026Article
- Toward Physiologically Relevant Organoid Models of Polycystic Kidney Disease through Microenvironment Reconstruction.Journal of the American Society of Nephrology : JASN · 2026Review
- Spatial Transcriptomics of the Cyst Microenvironment in an Autosomal Dominant Polycystic Kidney Disease Model.Journal of the American Society of Nephrology : JASN · 2026Article
- Spatial Transcriptomics Reveals Injured Cells, Signature Genes, and Communication Patterns in the Cyst Microenvironment of Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- Progressive endocannabinoid system dysregulation in autosomal dominant polycystic kidney disease.Molecular medicine (Cambridge, Mass.) · 2026Article
- Design of a configurable SoC for Alzheimer's disease detection based on multimodal signals.BMC bioinformatics · 2026Article
- Pellino1-mTOR/S6K1 signaling axis is a key pathogenesis for the development of polycystic kidney disease.Cell death & disease · 2026Article
- Immune microenvironment in autosomal dominant polycystic kidney disease.Genes & diseases · 2026Review
- Podocyte-Specific Deletion of STAT3 in Krüppel-Like Factor 4-Related Experimental Podocytopathy.Journal of the American Society of Nephrology : JASN · 2026Article
- Vascular transcriptional and metabolic changes precede progressive intrarenal microvascular rarefaction in autosomal dominant polycystic kidney disease.American journal of physiology. Renal physiology · 2026Article
- PAX gene expression in autosomal dominant polycystic kidney disease contributes to cyst expansion and regulates a gene network associated with cyst growth.Human molecular genetics · 2026Article
17 more citing papers are in PubMed but not listed here.
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18 authors at 3 institutions in 1 country.
Funding
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is the leading genetic cause of end stage renal disease characterized by progressive expansion of kidney cysts. To better understand the cell types and states driving ADPKD progression, we analyze eight ADPKD and five healthy human kidney samples, generating single cell multiomic atlas consisting of ~100,000 single nucleus transcriptomes and ~50,000 single nucleus epigenomes. Activation of proinflammatory, profibrotic signaling pathways are driven by proximal tubular cells with a failed repair transcriptomic signature, proinflammatory fibroblasts and collecting duct cells. We identify GPRC5A as a marker for cyst-lining collecting duct cells that exhibits increased transcription factor binding motif availability for NF-κB, TEAD, CREB and retinoic acid receptors. We identify and validate a distal enhancer regulating GPRC5A expression containing these motifs. This single cell multiomic analysis of human ADPKD reveals previously unrecognized cellular heterogeneity and provides a foundation to develop better diagnostic and therapeutic approaches.
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