ReviewCureus2025
Effects of Fibroblast Growth Factor 23 (FGF23) on the Cardiovascular System: A Review of Literature.
Review in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association between fibroblast growth factor 23 and coronary artery calcification in patients with chronic kidney disease: a meta-analysis.Frontiers in endocrinology · 2026Pooled it
- Beyond Creatinine: Novel Renal Biomarkers at the Interface of Kidney Injury and Cardiovascular Risk.Biomedicines · 2026Review
- Dietary Transitions and the Rising Global Burden of Chronic Kidney Disease: Insights from Nutritional Epidemiology.Nutrients · 2026Review
- Antiaging Properties of the Klotho Protein.Cells · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor 23 (FGF23) is a hormone that plays a crucial role in phosphate metabolism; its synthesis increases with phosphate intake. The effect of FGF23 is reduced by the decrease in Klotho protein in patients with chronic kidney disease (CKD). As a result, there is less phosphate excretion and, consequently, an increase in serum FGF23 levels. Several studies have shown that elevated FGF23 levels are associated with an increased risk of cardiovascular events. This is a consequence of the various alterations it causes at this level, including arterial stiffness, increased pulse wave velocity, left ventricular hypertrophy, cardiac tissue fibrosis, atrial fibrillation, and atherosclerosis, resulting in increased cardiovascular mortality and all-cause mortality. The pathophysiological mechanisms by which FGF23 generates all these alterations are novel and will be discussed in this review. Therapeutic strategies to reduce FGF23 levels include low-phosphate diets, some intestinal phosphate binders, calcimimetics, dialysis therapies, and some other medications that require further research to evaluate their effectiveness.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.