ArticleThe American journal of pathology2001
A vitamin D analog ameliorates glomerular injury on rat glomerulonephritis.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
48 citing papers in PubMed, 137 citations in OpenAlex.
- Trial
- Protective effects of vitamin DPharmaceutical biology · 2023Article
- Calcitriol Treatment Attenuates Uric Acid-Induced Kidney Injury via Super Oxide Dismutase-1 (SOD-1) Upregulation and Fibrosis ReductionIranian biomedical journal · 2021Article
- Nuclear receptors in podocyte biology and glomerular disease.Nature reviews. Nephrology · 2021Review
- Vitamin D and Glomerulonephritis.Medicina (Kaunas, Lithuania) · 2021Review
- Review
- A downstream molecule of 1,25-dihydroxyvitamin D3, alpha-1-acid glycoprotein, protects against mouse model of renal fibrosis.Scientific reports · 2018Article
- Article
- Differential expression and regulation of Klotho by paricalcitol in the kidney, parathyroid, and aorta of uremic rats.Kidney international · 2015Article
- Serum fibroblast growth factor-23 is associated with incident kidney disease.Journal of the American Society of Nephrology : JASN · 2015Article
- Role of Paricalcitol in Modulating the Immune Response in Patients with Renal Disease.International journal of endocrinology · 2015Article
- Article
- Vitamin D and chronic kidney disease.The Korean journal of internal medicine · 2014Review
- Cardiac and renal effects of atrasentan in combination with enalapril and paricalcitol in uremic rats.Kidney & blood pressure research · 2014Article
- Developments in renal pharmacogenomics and applications in chronic kidney disease.Pharmacogenomics and personalized medicine · 2014Review
- HIV compromises integrity of the podocyte actin cytoskeleton through downregulation of the vitamin D receptor.American journal of physiology. Renal physiology · 2013Article
- Anti-Thy-1 Antibody-mediated Complement-dependent Cytotoxicity is Regulated by the Distribution of Antigen, Antibody and Membrane Complement Regulatory Proteins in Rats.Journal of toxicologic pathology · 2013Article
- Pathogenesis and novel treatment from the mouse model of type 2 diabetic nephropathy.TheScientificWorldJournal · 2013Review
- Circulating vitamin D metabolites and kidney disease in type 1 diabetes.The Journal of clinical endocrinology and metabolism · 2012Article
- Nuclear hormone receptors in podocytes.Cell & bioscience · 2012Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
OCT (22-oxa-calcitriol), a vitamin D analog, has been reported to show strong inhibitory effects on mesangial cell proliferation in vitro. In the present study, we report a study of the effect of OCT on anti-thy-1 glomerulonephritis. Both OCT and 1,25(OH)(2)D(3) significantly inhibited mesangial cell proliferation, the degree of glomerulosclerosis, and albuminuria at day 8 compared to the disease control group. The OCT-treated group showed normal calcium levels but the 1,25(OH)(2)D(3)-treated group showed higher levels. The disease control group showed a marked increase of type I and type IV collagens, and alpha-smooth muscle actin (alpha-SMA) compared to the normal group. The treatment of OCT or 1,25(OH)(2)D(3) significantly reduced the expression of these proteins. The mRNA of the glomeruli of anti-thy-1 model expressed significantly higher levels of type I and type IV collagens, and alpha-SMA at day 8 compared to normal rats. Treatment with OCT or 1,25(OH)(2)D(3) inhibited the mRNA expressions of type I and type IV collagens, as well as that of alpha-SMA. These data demonstrate that OCT inhibits mesangial cell proliferation and extracellular matrix expansion with a low calcemic activity. Disease control rats showed significantly increased levels of transforming growth factor-beta1 protein in the glomeruli, but treatment with OCT or 1,25(OH)(2)D(3) markedly reduced this expression. The levels of mRNA in glomeruli were also consistent with these protein levels. Therefore, the suppressive effect of OCT may be mediated by inhibition of transforming growth factor-beta1. The present results suggest that OCT has potential for use in therapeutic strategy for the treatment of glomerulonephritis without inducing hypercalcemia.
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