ReviewBone2017
Cardiac actions of fibroblast growth factor 23.
Review in Bone, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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
35 citing papers in PubMed, 63 citations in OpenAlex.
- Post-transplant atrial tachyarrhythmias: Epidemiology, mechanisms, outcomes, and management across solid organs.World journal of transplantation · 2026Review
- Integrated MicroRNA-mRNA Sequencing Analysis Identifies Regulators and Networks Involved in Feline Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2025Article
- Vitamin D-Parathyroid Hormone-Fibroblast Growth Factor 23 Axis and Cardiac Remodeling.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2025Review
- Integrated Genomic Approaches to Elucidate the Genetic Basis of Brugada Syndrome in Taiwanese Patients.Bioinformatics and biology insights · 2025Article
- Machine learning-driven diagnostic signature provides new insights in clinical management of hypertrophic cardiomyopathy.ESC heart failure · 2024Article
- A robust cis-Mendelian randomization method with application to drug target discovery.Nature communications · 2024Article
- Growth factors and their roles in cardiac development and regeneration: a narrative review.Pediatric medicine (Hong Kong, China) · 2023Article
- A network medicine approach to study comorbidities in heart failure with preserved ejection fraction.BMC medicine · 2023Article
- Relationship of Fibroblast Growth Factor 23 With Hospitalization for Heart Failure and Cardiovascular Outcomes in Patients Undergoing Cardiac Surgery.Journal of the American Heart Association · 2023Article
- Hypertrophic cardiomyopathy in a patient with secondary hypoparathyroidism: A case report.Radiology case reports · 2022Article
- Silencing Survivin: a Key Therapeutic Strategy for Cardiac Hypertrophy.Journal of cardiovascular translational research · 2022Article
- A bioinformatics approach for identifying potential molecular mechanisms and key genes involved in COVID-19 associated cardiac remodeling.Gene reports · 2021Article
- High FGF23 Levels Failed to Predict Cardiac Hypertrophy in Animal Models of Hyperphosphatemia and Chronic Renal Failure.Journal of the Endocrine Society · 2021Article
- Change in Cardiac Biomarkers and Risk of Incident Heart Failure and Atrial Fibrillation in CKD: The Chronic Renal Insufficiency Cohort (CRIC) Study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2021Observational
- The relationship between Fibroblast Growth Factor 23 (FGF23) and cardiac MRI findings following primary PCI in patients with acute first time STEMI.International journal of cardiology. Heart & vasculature · 2021Article
- Targeting 5-HTCirculation · 2021Article
- Hypophosphataemia, fibroblast growth factor 23 and third-generation intravenous iron compounds: a narrative review.Drugs in context · 2021Review
- An Overview of FGF-23 as a Novel Candidate Biomarker of Cardiovascular Risk.Frontiers in physiology · 2021Review
- Fibroblast growth factor 23: a biomarker of fibrosis and prognosis in heart failure with preserved ejection fraction.ESC heart failure · 2020Article
- Association between plasma fibroblast growth factor 23 and left ventricular mass index in patients with Takayasu arteritis.Clinical rheumatology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Fibroblast growth factors (FGF) are mitogenic signal mediators that induce cell proliferation and survival. Although cardiac myocytes are post-mitotic, they have been shown to be able to respond to local and circulating FGFs. While precise molecular mechanisms are not well characterized, some FGF family members have been shown to induce cardiac remodeling under physiologic conditions by mediating hypertrophic growth in cardiac myocytes and by promoting angiogenesis, both events leading to increased cardiac function and output. This FGF-mediated physiologic scenario might transition into a pathologic situation involving cardiac cell death, fibrosis and inflammation, and eventually cardiac dysfunction and heart failure. As discussed here, cardiac actions of FGFs - with the majority of studies focusing on FGF2, FGF21 and FGF23 - and their specific FGF receptors (FGFR) and precise target cell types within the heart, are currently under experimental investigation. Especially cardiac effects of endocrine FGFs entered center stage over the past five years, as they might provide communication routes that couple metabolic mechanisms, such as bone-regulated phosphate homeostasis, or metabolic stress, such as hyperphosphatemia associated with kidney injury, with changes in cardiac structure and function. In this context, it has been shown that elevated serum FGF23 can directly tackle cardiac myocytes via FGFR4 thereby contributing to cardiac hypertrophy in models of chronic kidney disease, also called uremic cardiomyopathy. Precise characterization of FGFs and their origin and regulation of expression, and even more importantly, the identification of the FGFR isoforms that mediate their cardiac actions should help to develop novel pharmacological interventions for heart failure, such as FGFR4 inhibition to tackle uremic cardiomyopathy.
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What OpenQuestion 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 OpenQuestion graph.