ArticleAmerican journal of hypertension2014
Paricalcitol downregulates myocardial renin-angiotensin and fibroblast growth factor expression and attenuates cardiac hypertrophy in uremic rats.
Article in American journal of hypertension, 2014. 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, 50 citations in OpenAlex.
- A randomized intervention study to evaluate the effect of calcitriol therapy on the renin-angiotensin system in diabetes.Journal of the renin-angiotensin-aldosterone system : JRAASTrial
- Experimental rodent models of cardiorenal syndrome types 3 and 4: Insights and clinical relevance (Review).International journal of molecular medicine · 2026Review
- Association Between Calcium Supplementation and Recurrence of Cardiovascular Events in Patients With Cardiovascular Disease: A Population-Based Cohort Study.Journal of the American Heart Association · 2026Article
- Calcitriol Concentration in the Early Phase of Myocardial Infarction and Its Relation to Left Ventricular Ejection Fraction.Metabolites · 2024Article
- A robust cis-Mendelian randomization method with application to drug target discovery.Nature communications · 2024Article
- Vitamin D and Cardiovascular Diseases: An Update.Cureus · 2023Review
- Review
- Article
- Paricalcitol Attenuates Metabolic Syndrome-Associated Heart Failure through Enhanced Mitochondrial Fusion.Oxidative medicine and cellular longevity · 2022Article
- Review
- Vitamin D Effects on Bone Homeostasis and Cardiovascular System in Patients with Chronic Kidney Disease and Renal Transplant Recipients.Nutrients · 2021Review
- Fibroblast Growth Factor 23 and Left Ventricular Hypertrophy in Chronic Kidney Disease-A Pediatric Perspective.Frontiers in pediatrics · 2021Review
- Beneficial effects of paricalcitol on cardiac dysfunction and remodelling in a model of established heart failure.British journal of pharmacology · 2020Article
- FGF23-Mediated Activation of Local RAAS Promotes Cardiac Hypertrophy and Fibrosis.International journal of molecular sciences · 2019Article
- Article
- Cardioprotective Effects of Paricalcitol Alone and in Combination With FGF23 Receptor Inhibition in Chronic Renal Failure: Experimental and Clinical Studies.American journal of hypertension · 2019Article
- Shengmai Injection Suppresses Angiotensin II-Induced Cardiomyocyte Hypertrophy and ApoptosisFrontiers in pharmacology · 2019Article
- Vitamin D Receptor: A Novel Therapeutic Target for Kidney Diseases.Current medicinal chemistry · 2018Review
- Vitamin D treatment attenuates cardiac FGF23/FGFR4 signaling and hypertrophy in uremic rats.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017Article
- Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundVitamin D attenuates uremic cardiac hypertrophy, possibly by suppressing the myocardial renin-angiotensin system (RAS) and fibroblast growth factors (FGFs). We compared the suppression of cardiac hypertrophy and myocardial expression of RAS and FGF receptor genes offered by the vitamin D analog paricalcitol (Pc) or the angiotensin-converting enzyme inhibitor enalapril (E) in experimental uremia.
methodsRats with 5/6 nephrectomy received Pc or E for 8 weeks. Renal function, systolic blood pressure, and cardiac hypertrophy were evaluated. Myocardial expression of RAS genes, brain natriuretic peptide (BNP), and FGF receptor-1 (FGFR-1) were determined using quantitative reverse-transcription (pRT)-PCR.
resultsBlood pressure, proteinuria, and serum creatinine were significantly higher in untreated uremic animals. Hypertension was significantly reduced by E but only modestly by Pc; however, cardiac hypertrophy in the untreated group was similarly attenuated by Pc or E. Upregulation of myocardial expressions of renin, angiotensinogen, FGFR-1, and BNP in untreated uremic animals was reduced similarly by Pc and E, while the angiotensin II type 1 receptor was downregulated only by E.
conclusionsUremic cardiac hypertrophy is associated with activation of the myocardial RAS and the FGFR-1. Downregulation of these genes induced by Pc and E results in similar amelioration of left ventricular hypertrophy despite the different antihypertensive effects of these drugs.
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