ArticleKidney international2009
Combination therapy with paricalcitol and trandolapril reduces renal fibrosis in obstructive nephropathy.
Article in Kidney international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 74 citations in OpenAlex.
- Attenuating amiodarone-induced lung toxicity by the vitamin D receptor activator paricalcitol in rats: targeting TLR4/NF-κB/HIF-1α and TGF-β/Smad signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Review
- Farnesylthiosalicylic Acid-Loaded Albumin Nanoparticle Alleviates Renal Fibrosis by Inhibiting Ras/Raf1/p38 Signaling Pathway.International journal of nanomedicine · 2021Article
- Signaling Pathways Involved in Diabetic Renal Fibrosis.Frontiers in cell and developmental biology · 2021Review
- Egr1 Knockdown Combined with an ACE Inhibitor Ameliorates Diabetic Kidney Disease in Mice: Blockade of Compensatory Renin Increase.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Article
- Blockade of ERK1/2 by U0126 alleviates uric acid-induced EMT and tubular cell injury in rats with hyperuricemic nephropathy.American journal of physiology. Renal physiology · 2019Article
- Naringenin Ameliorates Renovascular Hypertensive Renal Damage by Normalizing the Balance of Renin-Angiotensin System Components in Rats.International journal of medical sciences · 2019Article
- The Signaling of Cellular Senescence in Diabetic Nephropathy.Oxidative medicine and cellular longevity · 2019Review
- Article
- Osthole Ameliorates Renal Fibrosis in Mice by Suppressing Fibroblast Activation and Epithelial-Mesenchymal Transition.Frontiers in physiology · 2018Article
- Inflammasome-Independent Role of NLRP3 Mediates Mitochondrial Regulation in Renal Injury.Frontiers in immunology · 2018Article
- Article
- Sustained Activation of Wnt/β-Catenin Signaling Drives AKI to CKD Progression.Journal of the American Society of Nephrology : JASN · 2016Article
- Wnt/β-catenin signaling and renin-angiotensin system in chronic kidney disease.Current opinion in nephrology and hypertension · 2016Review
- Article
- Vitamin D and the Epithelial to Mesenchymal Transition.Stem cells international · 2016Review
- Protective effect of Huang Gan formula in 5/6 nephrectomized rats by depressing the Wnt/β-catenin signaling pathway.Drug design, development and therapy · 2015Article
- Multiple genes of the renin-angiotensin system are novel targets of Wnt/β-catenin signaling.Journal of the American Society of Nephrology : JASN · 2015Article
- Kinin B1 receptor antagonism is equally efficient as angiotensin receptor 1 antagonism in reducing renal fibrosis in experimental obstructive nephropathy, but is not additive.Frontiers in pharmacology · 2015Article
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3 authors at 2 institutions in 2 countries.
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Abstract
Growing evidence suggests that active vitamin D slows the progression of chronic kidney diseases. Here we compared the individual renal protective efficacy of paricalcitol and trandolapril (an angiotensin-converting enzyme inhibitor) in obstructive nephropathy, and examined any potential additive effects of their combination on attenuating renal fibrosis and inflammation. Mice underwent unilateral ureteral obstruction and were treated individually with paricalcitol or trandolapril or their combination. Compared to vehicle-treated controls, monotherapy with paricalcitol or trandolapril inhibited the expression and accumulation of fibronectin and type I and type III collagen, suppressed alpha-smooth muscle actin, vimentin, and Snail1 expression, and reduced total collagen content in the obstructed kidney. Combination therapy led to a more profound inhibition of all parameters. Monotherapy also suppressed renal RANTES (regulated on activation, normal T cell expressed and secreted) and tumor necrosis factor (TNF)-alpha expression and inhibited renal infiltration of T cells and macrophages, whereas the combination had additive effects. Renin expression was induced in the fibrotic kidney and was augmented by trandolapril. Paricalcitol blocked renin induction in the absence or presence of trandolapril. Our study indicates that paricalcitol has renal protective effects, comparable to that of trandolapril, in reducing interstitial fibrosis and inflammation. Combination therapy had additive efficacy in retarding renal scar formation during obstructive nephropathy.
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