ArticleKidney international2016
Endostatin and transglutaminase 2 are involved in fibrosis of the aging kidney.
Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Ageing impacts extracellular matrix turnover and remodelling in the kidney.Matrix biology plus · 2026Article
- Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026Review
- Anti-Angiogenic Features of Endostatin in Obesity, Liver Fibrosis, and Hepatocellular Carcinoma.Biomedicines · 2026Review
- A rat model of Immunologic and hypertensive kidney injury.Scientific reports · 2026Article
- Hyperglycaemia-induced molecular reprogramming of proximal tubular epithelial cells and its contribution to diabetic kidney disease progression-a narrative review.Frontiers in cell and developmental biology · 2026Review
- Regulation of transglutaminase-2 and related miRNAs expression by calorie restriction in aorta of aging female mice.Molecular biology reports · 2025Article
- A Comprehensive Multiomics Signature of Doxorubicin-Induced Cellular Senescence in the Postmenopausal Human Ovary.Aging cell · 2025Article
- Permissive role of vascular endothelium in fibrosis: focus on the kidney.American journal of physiology. Cell physiology · 2024Review
- Immuno-Sensing at Ultra-Low Concentration of TG2 Protein by Organic Electrochemical Transistors.Biosensors · 2023Article
- A transcriptomic pan-cancer signature for survival prognostication and prediction of immunotherapy response based on endothelial senescence.Journal of biomedical science · 2023Article
- Proteolysis: a key post-translational modification regulating proteoglycans.American journal of physiology. Cell physiology · 2022Review
- Results of untargeted analysis using the SOMAscan proteomics platform indicates novel associations of circulating proteins with risk of progression to kidney failure in diabetes.Kidney international · 2022Article
- Application of a Fluorescence Anisotropy-Based Assay to Quantify Transglutaminase 2 Activity in Cell Lysates.International journal of molecular sciences · 2022Article
- Endostatin in Renal and Cardiovascular Diseases.Kidney diseases (Basel, Switzerland) · 2021Review
- Anti-Fibrotic Activity of an Antimicrobial Peptide in a Drosophila Model.Journal of innate immunity · 2021Article
- Peritubular Capillary Rarefaction: An Underappreciated Regulator of CKD Progression.International journal of molecular sciences · 2020Review
- Targeting angiogenesis and lymphangiogenesis in kidney disease.Nature reviews. Nephrology · 2020Review
- Cellular Senescence and Senotherapies in the Kidney: Current Evidence and Future Directions.Frontiers in pharmacology · 2020Review
- Extracellular Matrix in Kidney Fibrosis: More Than Just a Scaffold.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Review
- Tissue Transglutaminase-Mediated AT1 Receptor Sensitization Underlies Pro-inflammatory Cytokine LIGHT-Induced Hypertension.American journal of hypertension · 2019Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Endostatin (EST), an antiangiogenic factor, is enriched in aging kidneys. EST is also an interactive partner of transglutaminase 2 (TG2), an enzyme that cross-links extracellular matrix proteins. Here we tested whether EST and TG2 play a role in the fibrosis of aging. In wild-type mice, aging kidneys exhibited a 2- to 4-fold increase in TG2 paralleled by increased cross-linked extracellular matrix proteins and fibrosis. Mice transgenic to express EST showed renal fibrosis at a young age. One-month delivery of EST via minipumps to young mice showed increased renal fibrosis that became more robust when superimposed on folic acid-induced nephropathy. Upregulated TG2 and impaired renal function were apparent with EST delivery combined with folic acid-induced nephropathy. Subcapsular injection of TG2 and/or EST into kidneys of young mice not only induced interstitial fibrosis, but also increased the proportion of senescent cells. Thus, kidney fibrosis in aging may represent a natural outcome of upregulated EST and TG2, but more likely it appears to be a result of cumulative stresses occurring on the background of synergistically acting geronic (aging) proteins, EST and TG2.
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Registered trials
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