ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Single Cell and Spatial Transcriptomics Define a Proinflammatory and Profibrotic Niche After Kidney Injury.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Tenascin C-Derived Peptide 6 Promotes De Novo Kidney Regeneration after Partial Nephrectomy in Axolotl.Journal of the American Society of Nephrology : JASN · 2026Article
- The Lactate-lactylation circuitry in kidney fibrosis: cellular crosstalk from tubular metabolic reprogramming to macrophage effector functions.Seminars in immunopathology · 2026Review
- Mechanisms of Obesity-Related Kidney Disease: From Adipose Depot Biology to the Chymase-Aldosterone and Ghrelin-Leptin Axes.Biomolecules · 2026Review
- Single-cell RNA sequencing and spatial transcriptomics in the discovery of kidney disease potential biomarkers: a narrative review.BMC nephrology · 2026Review
- Tenascin C promotes the formation of abdominal aortic aneurysm by regulating the homeostasis of vascular smooth muscle cells.Biology direct · 2026Article
- iMSC-secreted factors preserve renal capillary networks and ameliorate fibrosis by interrupting the macrophage STING/CD8Stem cell research & therapy · 2026Article
- Stem cell therapies to modulate harmful immune responses in kidney disease: progress toward clinical validation.Stem cells (Dayton, Ohio) · 2026Review
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Beyond the Cell Atlas: Functional Communities as the Essential Pathologic Units Driving Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Review
- Cross-Talk Between Pyroptosis and Ferroptosis Promotes Intestinal Inflammation and Barrier Failure During PEDV Infection.Biomolecules · 2026Article
- Integration of multi-omics and network toxicology reveals TLR4-mediated nephrotoxicity induced by arecoline.BMC pharmacology & toxicology · 2026Article
- Computational Lymphocyte Topology: A Roadmap to Mechanism and Clinical Translation?Journal of the American Society of Nephrology : JASN · 2026Article
- A facile polysaccharide hydrogel activates PPARγ via the Gut-Kidney axis to ameliorate chronic kidney disease.Journal of nanobiotechnology · 2026Article
- Single Cell and Spatial Transcriptomics Define a Proinflammatory and Profibrotic Niche After Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Microbiota-associated metabolic networks in gut-kidney communication and renal immune regulation: mechanisms and therapeutic potential.Frontiers in microbiology · 2026Review
- Fibrillin-1 Orchestrates a Pro-senescent Niche Driving Peritubular Endothelial Senescence via ZEB1/endothelin-1/β-catenin Signaling.International journal of biological sciences · 2026Article
- Enhanced miR-214 in Vascular Endothelial Cells Retards Renal Inflammation and Glomerular Sclerosis in Five-Sixths Nephrectomy Mice.Kidney diseases (Basel, Switzerland)Article
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15 authors.
Funding
Abstract
Kidney fibrosis is the common outcome of chronic kidney disease (CKD). It often instigates in the focal sites by forming the fibrogenic niche after injury. In this study, using single-cell RNA sequencing (scRNA-seq) and a spatial transcriptomic (ST) approach, the cellular heterogeneity, spatial organization, and molecular interactions are delineated in the fibrotic kidney. Through analyses of the scRNA-seq and ST data from normal and fibrotic kidneys in mice subjected to unilateral ischemia-reperfusion injury, a tenascin C (TNC)-enriched, proinflammatory, and profibrotic microenvironment is identified that facilitated macrophage activation and promoted renal inflammation and fibrosis. Both TNC-enriched decellularized kidney tissue scaffold and exogenous TNC protein promoted bone marrow-derived macrophages activation though Toll-like receptor 4 (TLR4)/NF-κB signaling. Either pharmacological inhibition of TLR4 signaling or genetic knockout of its gene alleviated renal inflammation and fibrosis by inhibiting macrophage activation in vivo. Finally, chimeric mice that received bone marrow transplantation from TLR4-deficient donors are protected against kidney inflammation and fibrosis. These results suggest that TNC plays a crucial role in orchestrating the formation of a proinflammatory and profibrotic niche that promotes renal inflammation and fibrosis by activating macrophages via TLR4/NF-κB signaling. The findings underscore the complex interplay among fibroblasts, extracellular microenvironment, and macrophages that drive kidney fibrosis.
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