ArticleJournal of the American Society of Nephrology : JASN2026
Spatial Transcriptomics Reveals Injured Cells, Signature Genes, and Communication Patterns in the Cyst Microenvironment of Polycystic Kidney Disease.
Article in Journal of the American Society of Nephrology : JASN, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Collecting Duct-Targeted Lipid Nanoparticles DeliverbioRxiv : the preprint server for biology · 2026Article
- Beyond the Cell Atlas: Functional Communities as the Essential Pathologic Units Driving Kidney Disease.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
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7 authors.
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Abstract
key pointsMyofibroblasts and injury repair-related cell types were exclusively observed in polycystic kidney disease and enriched within the cyst microenvironment. Cyst-associated gene signature of 45 genes with decreased expression further away from the cysts was largely related to inflammation. Communication in low-inflamed cystic microdomains related to cellular signaling, morphogenesis, and inflammation in polycystic kidney disease.
backgroundChanges in the cyst microenvironment in polycystic kidney disease (PKD) may drive progressive cyst formation. Bulk-cell and single-cell RNA sequencing have advanced our understanding of altered signaling; however, the lack of spatial information has limited our insights into local gene expression and cellular communication near cysts.
methodsWe used wild-type and Pkd1 -deficient mouse kidneys to generate 10× Genomics Visium Spatial Gene Expression datasets. Using our single-cell mouse kidney atlas and single-cell sequencing data for spot deconvolution, we enhanced resolution and estimated enriched cell types. We analyzed spatial gene expression patterns and used a cyst-centered analysis to identify cyst-associated gene signature. Cell communication near cysts was investigated, identifying key ligand-receptors. Prioritized key factors were validated in tissues.
resultsWe observed enrichment of fibroblasts, injury repair-related cell types, and diverse immune populations in PKD. Injury repair-related cells were exclusively observed in PKD, predominantly localized within immune cell-dense regions near cysts. These cells collectively contributed to the altered gene expression profile in PKD, including cyst-associated signature genes related to inflammatory processes. Analysis of cellular communication in less-inflamed regions around cysts revealed the involvement of multiple cell types. Key ligand-receptor interactions were associated with cytokine signaling, fibrosis, cellular development, and repair. These included Angpt2 , C3 , Csf1 , Cxcl12 , Il34 , Gas6 , Il16 , Mdk , Mif , Ptn , Sfrp2 , Spp1 , Sdc1 , Tnc , Tnfsf12 , and Wnt5a . In addition, extracellular matrix (ECM) proteins implicated in immune response, ECM remodeling, cell adhesion, and cell signaling were identified, such as Adam9 , Adam10 , Col1a1, Col3a1, Col4a2, Lamb2, Lamc1, Efnb1 , Efnb2 , Thbs1, Thbs2 , and Vcam1 . Immunohistochemistry confirmed expression of Syndecan-1-Collagen IV, Midkine-Integrin β 1, CSF-1, Pleiotrophin, and Tenascin-C in cystic kidneys.
conclusionsSpatial transcriptomics in PKD revealed enrichment of (myo)fibroblasts, immune, and injury repair-related cells near cysts, creating a (pro)inflammatory and (pro)fibrotic niche. Key ligand-receptor and ECM interactions were identified and validated.
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