ArticleKidney international2019
Tenascin-C protects against acute kidney injury by recruiting Wnt ligands.
Article in Kidney international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 54 citations in OpenAlex.
- Targeting a Novel AREGCell proliferation · 2026Article
- From Mechanism to Therapy: Establishing an Integrated Framework for the Regulation and Intervention of Matrix Vesicles in Vascular Calcification.Cardiovascular drugs and therapy · 2026Review
- Sustained tenascin-C activation drives AKI-to-CKD progression via the Wnt/β-catenin pathway.International urology and nephrology · 2026Article
- Tenascin C-Derived Peptide 6 Promotes De Novo Kidney Regeneration after Partial Nephrectomy in Axolotl.Journal of the American Society of Nephrology : JASN · 2026Article
- Protective Effects and Mechanisms of Extracellular Vesicles in Remote Ischemic Preconditioning on Renal Injury Induced by Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Optimizing Early Detection of Diabetic Kidney Disease through Synergistic Biomarkers and Serum Metabolites in Humans.Diabetes & metabolism journal · 2026Article
- Podocyte-Derived Extracellular Vesicles Induce Endothelial Dysfunction by Triggering ER Stress in Glomerular Disease.Journal of extracellular vesicles · 2026Article
- Matricellular protein SMOC2 safeguards tubular integrity in acute kidney injury via integrin β3-dependent inhibition of CCND1-CDK4/6 axis.Molecular biomedicine · 2026Article
- Tenascin-C as a predictor of delayed graft function after kidney transplantation.Frontiers in immunology · 2026Article
- Single Cell and Spatial Transcriptomics Define a Proinflammatory and Profibrotic Niche After Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fibroblast activation and heterogeneity in fibrotic disease.Nature reviews. Nephrology · 2025Review
- Tenascin-C Potentiates Wnt Signaling in Thyroid Cancer.Endocrinology · 2025Article
- Lipin3 deficiency aggravates cisplatin induced acute kidney injury via activating Sirt1-p21-Caspase 3-GSDME pyroptosis pathway.International journal of biological sciences · 2025Article
- β-catenin-inhibited Sumoylation modification of LKB1 and fatty acid metabolism is critical in renal fibrosis.Cell death & disease · 2024Article
- FAM3A plays a key role in protecting against tubular cell pyroptosis and acute kidney injury.Redox biology · 2024Article
- Tenascin C activates the toll‑like receptor 4/NF‑κB signaling pathway to promote the development of polycystic ovary syndrome.Molecular medicine reports · 2024Article
- Article
- Cell-cell communication in kidney fibrosis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Review
- Biology of Tenascin C and its Role in Physiology and Pathology.Current medicinal chemistry · 2024Review
- Tenascin-C promotes the proliferation and fibrosis of mesangial cells in diabetic nephropathy through the β-catenin pathway.International urology and nephrology · 2023Review
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
The development of acute kidney injury (AKI) is a complex process involving tubular, inflammatory, and vascular components, but less is known about the role of the interstitial microenvironment. We have previously shown that the extracellular matrix glycoprotein tenascin-C (TNC) is induced in fibrotic kidneys. In mouse models of AKI induced by ischemia-reperfusion injury (IRI) or cisplatin, TNC was induced de novo in the injured sites and localized to the renal interstitium. The circulating level of TNC protein was also elevated in AKI patients after cardiac surgery. Knockdown of TNC by shRNA in vivo aggravated AKI after ischemic or toxic injury. This effect was associated with reduced renal β-catenin expression, suggesting an impact on Wnt signaling. In vitro, TNC protected tubular epithelial cells against apoptosis and augmented Wnt1-mediated β-catenin activation. Co-immunoprecipitation revealed that TNC physically interacts with Wnt ligands. Furthermore, a TNC-enriched kidney tissue scaffold prepared from IRI mice was able to recruit and concentrate Wnt ligands from the surrounding milieu ex vivo. The ability to recruit Wnt ligands in this ex vivo model diminished after TNC depletion. These studies indicate that TNC is specifically induced at sites of injury and recruits Wnt ligands, thereby creating a favorable microenvironment for tubular repair and regeneration after AKI.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.