ReviewMolecular metabolism2026
Fibroblast growth factor 23: Regulation, signalling and systemic links between bone, metabolism and inflammation.
Review in Molecular metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor 23 (FGF23) is a bone-derived hormone and growth factor that plays a central role in phosphate and mineral homeostasis. Beyond its classical endocrine actions on the kidney, accumulating evidence indicates that FGF23 exerts broad paracrine and systemic effects that extend to metabolism, inflammation, cardiovascular function and cancer biology. FGF23 production is tightly regulated at the transcriptional and post-translational levels in osteocytes and osteoblasts, resulting in the release of either intact bioactive FGF23 or cleaved fragments with distinct biological properties. Canonical FGF23 signalling requires fibroblast growth factor receptors in complex with the co-receptor α-Klotho, although α-Klotho-independent pathways have been described in several tissues. This review provides a comprehensive overview of FGF23 biology, focusing on its regulation, processing and signalling mechanisms, and integrating current knowledge of its paracrine and endocrine actions across multiple organ systems. We discuss the role of FGF23 in bone mineralisation, phosphocalcium metabolism and energy homeostasis, as well as its involvement in inflammatory states, anaemia, cardiovascular disease, chronic kidney disease, cancer and nervous system function. Experimental and clinical evidence supporting both adaptive and maladaptive roles of FGF23 in health and disease is critically examined. Overall, FGF23 emerges as a multifunctional growth factor and hormone that links bone to systemic metabolic and inflammatory networks. Understanding the context-dependent actions of FGF23 may provide novel insights into disease mechanisms and identify new opportunities for therapeutic intervention.
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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.