ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2018
Genetic background influences cardiac phenotype in murine chronic kidney disease.
Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2018. 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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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
27 citing papers in PubMed, 36 citations in OpenAlex.
- Estrogen protects female mice with chronic kidney disease from fibroblast growth factor 23-induced left ventricular hypertrophy.Kidney international · 2026Article
- Transgenic augmentation of erythroferrone in mice ameliorates anemia in adenine-induced chronic kidney disease.JCI insight · 2025Article
- Cardiorenal syndrome: clinical diagnosis, molecular mechanisms and therapeutic strategies.Acta pharmacologica Sinica · 2025Review
- Disease-modifying effects of iron deficiency in mouse models of chronic renal failure.Blood red cells & iron · 2025Article
- Fibroblast growth factor 23 and fibroblast growth factor receptor 4 promote cardiac metabolic remodeling in chronic kidney disease.Kidney international · 2025Article
- Enhancing gene transfer to renal tubules and podocytes by context-dependent selection of AAV capsids.Nature communications · 2024Article
- In chronic kidney disease altered cardiac metabolism precedes cardiac hypertrophy.American journal of physiology. Renal physiology · 2024Article
- Fibroblast Growth Factor (FGF) 23 and FGF Receptor 4 promote cardiac metabolic remodeling in chronic kidney disease.Research square · 2023Article
- Transcription factor HNF4α2 promotes osteogenesis and prevents bone abnormalities in mice with renal osteodystrophy.The Journal of clinical investigation · 2023Article
- A Comparative Presentation of Mouse Models That Recapitulate Most Features of Alport Syndrome.Genes · 2022Review
- Article
- The Role of DMP1 in CKD-MBD.Current osteoporosis reports · 2021Review
- Lipocalin 2 stimulates bone fibroblast growth factor 23 production in chronic kidney disease.Bone research · 2021Article
- Article
- Inflammation: a putative link between phosphate metabolism and cardiovascular disease.Clinical science (London, England : 1979) · 2021Review
- Simultaneous management of disordered phosphate and iron homeostasis to correct fibroblast growth factor 23 and associated outcomes in chronic kidney disease.Current opinion in nephrology and hypertension · 2020Review
- Cardiac Remodeling in Chronic Kidney Disease.Toxins · 2020Review
- 5/6 nephrectomy induces different renal, cardiac and vascular consequences in 129/Sv and C57BL/6JRj mice.Scientific reports · 2020Article
- Soluble Epoxide Hydrolase Inhibition Prevents Experimental Type 4 Cardiorenal Syndrome.Frontiers in molecular biosciences · 2020Article
- Ferric citrate reduces fibroblast growth factor 23 levels and improves renal and cardiac function in a mouse model of chronic kidney disease.Kidney international · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Background: Levels of fibroblast growth factor 23 (FGF23) increase early in chronic kidney disease (CKD) and are independently associated with left ventricular hypertrophy (LVH), heart failure and death. Experimental models of CKD with elevated FGF23 and LVH are needed. We hypothesized that slow rates of CKD progression in the Col4a3 knockout (Col4a3KO) mouse model of CKD would promote development of LVH by prolonging exposure to elevated FGF23. Methods: We studied congenic Col4a3KO and wild-type (WT) mice with either 75% 129X1/SvJ (129Sv) or 94% C57Bl6/J (B6) genomes. Results: B6-Col4a3KO lived longer than 129Sv-Col4a3KO mice (21.4 ± 0.6 versus 11.4 ± 0.4 weeks; P < 0.05). 10-week-old 129Sv-Col4a3KO mice showed impaired renal function (blood urea nitrogen 191 ± 39 versus 34 ± 4 mg/dL), hyperphosphatemia (14.1 ± 1.4 versus 6.8 ± 0.3 mg/dL) and 33-fold higher serum FGF23 levels (P < 0.05 versus WT for each). Consistent with their slower CKD progression, 10 week-old B6-Col4a3KO mice showed milder impairment of renal function than 129Sv-Col4a3KO mice and modest FGF23 elevation without other alterations of mineral metabolism. At 20 weeks, further declines in renal function in B6-Col4a3KO mice was accompanied by hyperphosphatemia and 8-fold higher FGF23 levels (P < 0.05 versus WT for each). Only the 20-week-old B6-Col4a3KO mice developed LVH (LV mass 125 ± 3 versus 98 ± 6 mg; P < 0.05 versus WT) in association with significantly increased cardiac expression of FGF receptor 4 (FGFR4) messenger RNA and protein and markers of LVH (Atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), beta-myosin heavy chain (β-MHC); P < 0.05 versus WT for each). Conclusions: In conclusion, B6-Col4a3KO mice manifest slower CKD progression and longer survival than 129Sv-Col4a3KO mice and can serve as a novel model of cardiorenal disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.