Iron, inflammation, and fibroblast growth factor 23: Integrating molecular crosstalk, cardiovascular biology, and therapeutic perspectives

doi:10.5528/wjtm.127250

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World Journal of Translational Medicine

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2220-6132

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.

World J Transl Med. Nov 28, 2026; 12(4): 127250
Published online Nov 28, 2026. doi: 10.5528/wjtm.127250

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Figure 1 Iron-inflammation-erythropoiesis control of fibroblast growth factor 23 production and processing. Iron deficiency, inflammation, and erythropoietic stress increase fibroblast growth factor 23 production, whereas proteolytic processing determines the balance between intact fibroblast growth factor 23 and C-terminal fragments. FGF23: Fibroblast growth factor 23; HIF: Hypoxia-inducible factor; IL-6: Interleukin-6; TNFα: Tumor necrosis factor alpha; EPO: Erythropoietin; FGFR4: Fibroblast growth factor receptor 4; HF: Heart failure.

Citation: Donate-Correa J. Iron, inflammation, and fibroblast growth factor 23: Integrating molecular crosstalk, cardiovascular biology, and therapeutic perspectives. World J Transl Med 2026; 12(4): 127250
URL: https://www.wjgnet.com/2220-6132/full/v12/i4/127250.htm
DOI: https://dx.doi.org/10.5528/wjtm.127250

Donate-Correa J. Iron, inflammation, and fibroblast growth factor 23: Integrating molecular crosstalk, cardiovascular biology, and therapeutic perspectives. World J Transl Med 2026; 12(4): 127250 [DOI: 10.5528/wjtm.127250]

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