ArticleJournal of the American Society of Nephrology : JASN2026
Integrin α 1 β 1 Promotes Interstitial Fibrosis and Cyst Growth in a Mouse Model 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.
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- 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
- sc2DAT: workflow for targeting tumor subpopulations of single cells.Bioinformatics advances · 2025Article
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Abstract
key pointsMultiomic analysis of the Pkd1nl/nl mouse and human autosomal dominant polycystic kidney disease tissue identified upregulation of integrin- α 1. Global knockout of integrin subunit α 1 reduced kidney cyst size and preserved kidney function. Loss of integrin- α 1 in Pkd1nl/nl mice precluded interstitial fibrosis, which we suggest was due to reduced fibroblast cell proliferation.
backgroundCystogenesis and interstitial fibrosis are contributing factors to kidney failure in individuals with autosomal dominant polycystic kidney disease (ADPKD). The molecular and cellular mechanisms involved in cyst growth and fibrosis are complex, and new therapies are urgently needed to improve clinical outcomes.
methodsWe used mass spectrometry-based proteomics to identify molecular changes in the Pkd1nl/nl mouse model of ADPKD and selected integrin- α 1 as a candidate of interest to follow-up in functional studies. Mice lacking integrin- α 1 ( Itga1-/- ) were crossed to Pkd1nl/nl mice, and effects on kidney function and kidney histology were measured. We investigated the effects of integrin- α 1 depletion on fibrosis markers using quantitative RT-PCR, Western blot, and immunofluorescence.
resultsProteomic analysis of the Pkd1nl/nl mouse showed increased abundance of integrin- α 1. In human ADPKD tissue and two single-cell RNA kidney disease datasets, ITGA1 was also upregulated. To investigate the functional role of this integrin subunit in ADPKD, we generated a Pkd1nl/nlItga1-/- mouse. We observed a significant reduction in kidney volume and kidney dysfunction in Pkd1nl/nl mice lacking integrin- α 1. Kidneys from Pkd1nl/nlItga1-/- mice had smaller cysts, reduced interstitial expansion, and less tubular atrophy. The myofibroblast marker α -smooth muscle actin remained switched on in Pdgfrb + stromal cells of Pkd1nl/nlItga1-/- kidneys, suggesting that integrin- α 1 is not needed for activation of fibroblasts. Analysis of cell proliferation markers suggested that integrin- α 1 promoted fibroblast expansion in response to cystic injury.
conclusionsThese results highlight a previously unrecognized role for integrin- α 1 in cyst growth and fibrosis in PKD.
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