ArticleKidney international2023
Single nuclei transcriptomics delineates complex immune and kidney cell interactions contributing to kidney allograft fibrosis.
Article in Kidney international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Single-Nucleus Transcriptomic Atlas Reveals Disease-Associated Cellular States in Human Glomerular Diseases.Kidney international reports · 2026Article
- Next-generation kidney tissue analysis - spatial omics and digital pathology.Nature reviews. Nephrology · 2026Review
- Beyond the Cell Atlas: Functional Communities as the Essential Pathologic Units Driving Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Review
- A macrophage-endothelial cell axis in kidney diseases.International urology and nephrology · 2026Review
- Injured epithelial cell states impact kidney allograft survival after T-cell-mediated rejection.Nature communications · 2026Article
- Renal allograft interstitial fibrosis: multicellular interactions and therapeutic strategies.Frontiers in immunology · 2026Review
- Single-cell transcriptomic landscape of metabolic reprogramming in kidney allograft rejection.Frontiers in immunology · 2026Article
- Identification of lactylation and its hub genes in contributing immune activation and renal allograft fibrosis by integrative bioinformatics and machine learning.Frontiers in immunology · 2026Article
- Intragraft donor-specific antibodies reflect histologic heterogeneity in kidney allografts with concurrent serum DSA.Frontiers in immunology · 2026Article
- Targeted Expansion of Treg Cells to Induce Immune Tolerance after Kidney Transplantation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fibroblast activation and heterogeneity in fibrotic disease.Nature reviews. Nephrology · 2025Review
- Prospective evaluation of arterial spin labeling and diffusion tensor imaging-magnetic resonance imaging for the non-invasive assessment of renal allograft dysfunction.Quantitative imaging in medicine and surgery · 2025Article
- Epithelial-Immune-Stromal Interactions Define Divergent Repair and Fibrosis Pathways After Acute Kidney Injury in Human Renal Transplants.bioRxiv : the preprint server for biology · 2025Article
- Spatial transcriptomics of Glomerulo-centric antibody mediated rejection in renal transplants.Clinical immunology (Orlando, Fla.) · 2025Article
- Cellular and Molecular Resolution of Focal Segmental Glomerulosclerosis Recurrence in Human Allografts.bioRxiv : the preprint server for biology · 2025Article
- Novel insights into kidney disease: the scRNA-seq and spatial transcriptomics approaches: a literature review.BMC nephrology · 2025Review
- Mesenchymal cell-derived exosomes and miR-29a-3p mitigate renal fibrosis and vascular rarefaction after renal ischemia reperfusion injury.Stem cell research & therapy · 2025Article
- METTL3 Potentiates M2 Macrophage-Driven MMT to Aggravate Renal Allograft Fibrosis via the TGF-β1/Smad3 Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Single-Cell Analysis Provides New Insights into the Roles of Tertiary Lymphoid Structures and Immune Cell Infiltration in Kidney Injury and Chronic Kidney Disease.The American journal of pathology · 2025Review
- The single-cell revolution in transplantation: high-resolution mapping of graft rejection, tolerance, and injury.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Chronic allograft dysfunction (CAD), characterized histologically by interstitial fibrosis and tubular atrophy, is the major cause of kidney allograft loss. Here, using single nuclei RNA sequencing and transcriptome analysis, we identified the origin, functional heterogeneity, and regulation of fibrosis-forming cells in kidney allografts with CAD. A robust technique was used to isolate individual nuclei from kidney allograft biopsies and successfully profiled 23,980 nuclei from five kidney transplant recipients with CAD and 17,913 nuclei from three patients with normal allograft function. Our analysis revealed two distinct states of fibrosis in CAD; low and high extracellular matrix (ECM) with distinct kidney cell subclusters, immune cell types, and transcriptional profiles. Imaging mass cytometry analysis confirmed increased ECM deposition at the protein level. Proximal tubular cells transitioned to an injured mixed tubular (MT1) phenotype comprised of activated fibroblasts and myofibroblast markers, generated provisional ECM which recruited inflammatory cells, and served as the main driver of fibrosis. MT1 cells in the high ECM state achieved replicative repair evidenced by dedifferentiation and nephrogenic transcriptional signatures. MT1 in the low ECM state showed decreased apoptosis, decreased cycling tubular cells, and severe metabolic dysfunction, limiting the potential for repair. Activated B, T and plasma cells were increased in the high ECM state, while macrophage subtypes were increased in the low ECM state. Intercellular communication between kidney parenchymal cells and donor-derived macrophages, detected several years post-transplantation, played a key role in injury propagation. Thus, our study identified novel molecular targets for interventions aimed to ameliorate or prevent allograft fibrogenesis in kidney transplant recipients.
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