ArticleKidney international2013
Low nitric oxide bioavailability upregulates renal heparin binding EGF-like growth factor expression.
Article in Kidney international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Endothelial eNOS deficiency causes podocyte injury through NFAT2 and heparanase in diabetic mice.Scientific reports · 2024Article
- Review
- The critical role of the Hippo signaling pathway in kidney diseases.Frontiers in pharmacology · 2022Review
- Serial intravital imaging captures dynamic and functional endothelial remodeling with single-cell resolution.JCI insight · 2021Article
- The renal microcirculation in chronic kidney disease: novel diagnostic methods and therapeutic perspectives.Cell & bioscience · 2021Review
- Role of Heparin-Binding Epidermal Growth Factor-Like Growth Factor in Oxidative Stress-Associated Metabolic Diseases.Metabolic syndrome and related disorders · 2020Review
- Article
- Epidermal Growth Factor Receptor: A Potential Therapeutic Target for Diabetic Kidney Disease.Frontiers in pharmacology · 2020Review
- Role of Epidermal Growth Factor Receptor (EGFR) and Its Ligands in Kidney Inflammation and Damage.Mediators of inflammation · 2018Review
- Selective activation of epidermal growth factor receptor in renal proximal tubule induces tubulointerstitial fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Specific endothelial heparin-binding EGF-like growth factor deletion ameliorates renal injury induced by chronic angiotensin II infusion.American journal of physiology. Renal physiology · 2016Article
- The epidermal growth factor receptor pathway in chronic kidney diseases.Nature reviews. Nephrology · 2016Review
- Can we fight chronic kidney disease by targeting endothelial HB-EGF?American journal of physiology. Renal physiology · 2016Article
- Interaction of the EGF Receptor and the Hippo Pathway in the Diabetic Kidney.Journal of the American Society of Nephrology : JASN · 2016Article
- Excess HB-EGF, which promotes VEGF signaling, leads to hydrocephalus.Scientific reports · 2016Article
- ROCK1 Induces Endothelial-to-Mesenchymal Transition in Glomeruli to Aggravate Albuminuria in Diabetic Nephropathy.Scientific reports · 2016Article
- High Glucose Up-regulates ADAM17 through HIF-1α in Mesangial Cells.The Journal of biological chemistry · 2015Article
- EGF receptor deletion in podocytes attenuates diabetic nephropathy.Journal of the American Society of Nephrology : JASN · 2015Article
- Role of endothelial nitric oxide synthase in diabetic nephropathy: lessons from diabetic eNOS knockout mice.Journal of diabetes research · 2014Review
- A Case of Rapidly Progressive Diabetic Nephropathy Induced by Osimertinib.Case reports in nephrology and dialysisArticle
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Decreased nitric oxide bioavailability has an important role in the initiation and progression of diabetic nephropathy, but the underlying mechanisms remain unclear. Here, we found that heparin-binding epidermal growth factor-like growth factor (HB-EGF) expression levels increased in the kidneys of both endothelial nitric oxide synthase (eNOS)-knockout and eNOS-knockout diabetic (Lepr(db/db)) mice as early as at 8 weeks of age. Further increases in expression were only seen in eNOS-knockout diabetic mice and paralleled the progression of glomerulopathy. HB-EGF expression increased in endothelium, podocytes, and tubular epithelial cells. In cultured glomerular endothelial cells, the nitric oxide synthase inhibitors NG-nitro-L-arginine methyl ester (L-NAME) or L-N5-(1-iminoethyl) ornithine increased HB-EGF protein expression. Administration of L-NAME dramatically increased renal HB-EGF expression and urinary HB-EGF excretion in diabetic mice. On the other hand, replenishing nitric oxide with sodium nitrate in eNOS-knockout diabetic mice reduced urinary HB-EGF excretion and inhibited the progression of diabetic nephropathy. Furthermore, specific deletion of HB-EGF expression in the endothelium attenuated renal injury in diabetic eNOS-knockout mice. Thus, our results suggest that decreased nitric oxide bioavailability leads to increased HB-EGF expression, which may be an important mediator of the resulting progressive diabetic nephropathy in eNOS-knockout diabetic mice.
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