ArticleBritish journal of pharmacology2013
NFAT2 inhibitor ameliorates diabetic nephropathy and podocyte injury in db/db mice.
Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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51 citing papers in PubMed, 83 citations in OpenAlex.
- Diverse effects of calcineurin in vascular smooth muscle cells: physiological activators and the controversial actions of clinical inhibitors.Frontiers in pharmacology · 2026Review
- Article
- Mechanism of mesenchymal stem cells in treating diabetic kidney disease.Stem cell research & therapy · 2025Review
- Redirecting microglia phenotype via inhibition of NFAT1 ameliorates deficits in mouse model of synucleinopathies.Experimental & molecular medicine · 2025Article
- Unlocking the therapeutic potential of the NFAT pathway in kidney diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Circulating miRNA-486 as a novel diagnostic biomarker for right ventricular remodeling.Frontiers in cardiovascular medicine · 2025Article
- Placenta-derived mesenchymal stem cells protect against diabetic kidney disease by upregulating autophagy-mediated SIRT1/FOXO1 pathway.Renal failure · 2024Article
- Endothelial eNOS deficiency causes podocyte injury through NFAT2 and heparanase in diabetic mice.Scientific reports · 2024Article
- NFAT3-FasL axis synchronously regulates apoptosis and necroptosis in murine cochlear outer hair cells after noise trauma.Frontiers in molecular neuroscience · 2024Article
- CaMKII may regulate renal tubular epithelial cell apoptosis through YAP/NFAT2 in acute kidney injury mice.Renal failure · 2023Article
- Ameliorative Effects of Camel Milk and Its Exosomes on Diabetic Nephropathy in Rats.Membranes · 2022Article
- miRNA-486-5p: signaling targets and role in non-malignant disease.Cellular and molecular life sciences : CMLS · 2022Review
- Intrarenal arterial administration of human umbilical cord-derived mesenchymal stem cells effectively preserved the residual renal function of diabetic kidney disease in rat.Stem cell research & therapy · 2022Article
- Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4.Genes & diseases · 2022Article
- Signal transduction mechanism of exosomes in diabetic complications (Review).Experimental and therapeutic medicine · 2022Review
- Yi-Shen-Hua-Shi granules inhibit diabetic nephropathy by ameliorating podocyte injury induced by macrophage-derived exosomes.Frontiers in pharmacology · 2022Article
- The role of FOXO4/NFAT2 signaling pathway in dysfunction of human coronary endothelial cells and inflammatory infiltration of vasculitis in Kawasaki disease.Frontiers in immunology · 2022Article
- Integrin β3 overexpression contributes to podocyte injury through inhibiting RhoA/YAP signaling pathway.Bioengineered · 2021Article
- Circular RNA_0037128 aggravates high glucose-induced damage in HK-2 cells via regulation of microRNA-497-5p/nuclear factor of activated T cells 5 axis.Bioengineered · 2021Article
- GAP-43 ameliorates Podocyte injury by decreasing nuclear NFATc1 expression.Biochemistry and biophysics reports · 2021Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposePodocyte injury plays a key role in the development of diabetic nephropathy (DN). We have recently shown that 11R-VIVIT, an inhibitor of cell-permeable nuclear factor of activated T-cells (NFAT), attenuates podocyte apoptosis induced by high glucose in vitro. However, it is not known whether 11R-VIVIT has a protective effect on DN, especially podocyte injury, under in vivo diabetic conditions. Hence, we examined the renoprotective effects of 11R-VIVIT in diabetic db/db mice and the possible mechanisms underlying its protective effects on podocyte injury in vivo and in vitro. EXPERIMENTAL APPROACH: Type 2 diabetic db/db mice received i.p. injections of 11R-VIVIT (1 mg·kg(-1)) three times a week and were killed after 8 weeks. Immortalized mouse podocytes were cultured under different experimental conditions. KEY
results11R-VIVIT treatment markedly attenuated the albuminuria in diabetic db/db mice and also alleviated mesangial matrix expansion and podocyte injury. However, body weight, food and water intake, and glucose levels were unaffected. It also attenuated the increased NFAT2 activation and enhanced urokinase-type plasminogen activator receptor (uPA receptor) expression in glomerulor podocytes. In cultured podocytes, the increased nuclear accumulation of NFAT2 and uPA receptor expression induced by high glucose treatment was prevented by 11R-VIVIT or NFAT2-knockdown; this was accompanied by improvements in the filtration barrier function of the podocyte monolayer. CONCLUSIONS AND IMPLICATIONS: The NFAT inhibitor 11R-VIVIT might be a useful therapeutic strategy for protecting podocytes and treating DN. The calcinerin/NFAT2/uPA receptor signalling pathway should be exploited as a therapeutic target for protecting podocytes from injury in DN.
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