ArticleJCI insight2019
Increased FGF23 protects against detrimental cardio-renal consequences during elevated blood phosphate in CKD.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Therapeutic Targets for Heart Failure Identified Using Proteomics and Mendelian Randomization.Circulation · 2022Pooled it
- ETV1 Couples Reciprocal FGF23 and PTH Signaling to RenalResearch square · 2026Article
- Fibroblast growth factor 23: Regulation, signalling and systemic links between bone, metabolism and inflammation.Molecular metabolism · 2026Review
- Development of a nomogram for predicting incident heart failure and all-cause mortality in patients with chronic kidney disease: a 3-year follow-up study.Frontiers in medicine · 2026Article
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- Article
- SELENBP1 protects against kidney fibrosis in chronic kidney disease as a methanethiol oxidase.Science China. Life sciences · 2025Article
- [Potential of early diagnosis and targeted therapy for Klotho protein in chronic kidney disease].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Accelerated osteocytic citrate production in chronic kidney disease is associated with protection of the kidney.bioRxiv : the preprint server for biology · 2025Article
- Genetic deletion of the sodium phosphate cotransporter NaPi2a ameliorates heart failure in mice.Scientific reports · 2025Article
- The actin and microtubule network regulator WHAMM is identified as a key kidney disease risk gene.Cell reports · 2025Article
- Comment on "Multiomics Analysis Reveals Therapeutic Targets for Chronic Kidney Disease With Sarcopenia" by Wang et al.Journal of cachexia, sarcopenia and muscle · 2025Article
- C-terminal fragment of fibroblast growth factor 23 improves heart function in murine models of high intact fibroblast growth factor 23.American journal of physiology. Renal physiology · 2024Article
- Gα11 deficiency increases fibroblast growth factor 23 levels in a mouse model of familial hypocalciuric hypercalcemia.JCI insight · 2024Article
- Common mouse models of chronic kidney disease are not associated with cachexia.Communications biology · 2024Article
- Vascular, valvular and kidney calcification manifested in mouse models of adenine-induced chronic kidney disease.Renal failure · 2023Article
- Bone marrow sinusoidal endothelial cells are a site of Fgf23 upregulation in a mouse model of iron deficiency anemia.Blood advances · 2023Article
- Physiopathology of Phosphate Disorders.Advances in kidney disease and health · 2023Review
- Fibrosis: Types, Effects, Markers, Mechanisms for Disease Progression, and Its Relation with Oxidative Stress, Immunity, and Inflammation.International journal of molecular sciences · 2023Review
- Osteocyte Egln1/Phd2 links oxygen sensing and biomineralization via FGF23.Bone research · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
The phosphaturic hormone FGF23 is elevated in chronic kidney disease (CKD). The risk of premature death is substantially higher in the CKD patient population, with cardiovascular disease (CVD) as the leading mortality cause at all stages of CKD. Elevated FGF23 in CKD has been associated with increased odds for all-cause mortality; however, whether FGF23 is associated with positive adaptation in CKD is unknown. To test the role of FGF23 in CKD phenotypes, a late osteoblast/osteocyte conditional flox-Fgf23 mouse (Fgf23fl/fl/Dmp1-Cre+/-) was placed on an adenine-containing diet to induce CKD. Serum analysis showed casein-fed Cre+ mice had significantly higher serum phosphate and blood urea nitrogen (BUN) versus casein diet and Cre- genotype controls. Adenine significantly induced serum intact FGF23 in the Cre- mice over casein-fed mice, whereas Cre+ mice on adenine had 90% reduction in serum intact FGF23 and C-terminal FGF23 as well as bone Fgf23 mRNA. Parathyroid hormone was significantly elevated in mice fed adenine diet regardless of genotype, which significantly enhanced midshaft cortical porosity. Echocardiographs of the adenine-fed Cre+ hearts revealed profound aortic calcification and cardiac hypertrophy versus diet and genotype controls. Thus, these studies demonstrate that increased bone FGF23, although associated with poor outcomes in CKD, is necessary to protect against the cardio-renal consequences of elevated tissue phosphate.
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Registered trials
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