2026-09-14T22:08:24Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/275922026-07-17T00:16:14Zcom_20.500.12105_19586com_20.500.12105_2202col_20.500.12105_19587

00925njm 22002777a 4500 dc Vázquez-Sánchez, Sara author Blasco, Ana author Polo-Salguero, Marina author Mourino-Álvarez, Laura author Gil-Fernández, Marta author Corbacho-Alonso, Nerea author Navarro-García, José Alberto author Mercado-García, Elisa author González-Lafuente, Laura author Rodríguez-Sánchez, Elena author González-Moreno, Daniel author Pérez-Gómez, Alberto author Matutano, Andrea author Vázquez, Jesús author López, Juan Antonio author Fernández-Velasco, María author Barderas, María G author Ruiz-Hurtado, Gema author 2026-02-17 Elevation of FGF23 (fibroblast growth factor 23) and decreased Klotho levels have been associated with various cardiovascular and renal diseases. However, the combined study of the FGF23-Klotho axis in ischemic heart disease remains elusive. We analyzed the associations between circulating FGF23 and Klotho levels with cardiac and renal parameters, as well as mortality outcomes following myocardial infarction (MI). Cardiac tissue from patients with ischemic heart disease and a post-MI mouse model were analyzed to assess myocardial FGF23 expression. Proteomic analysis was performed to examine myocardial pathways activated by FGF23 and regulated by Klotho. We observed an inverse correlation between circulating levels of FGF23 and Klotho in patients after MI. Elevated plasma FGF23 levels were particularly associated with ST-segment-elevation MI and cardiac dysfunction, including reduced left ventricular ejection fraction, prolonged corrected interval, and higher Killip-Kimball classification of cardiac risk, identifying FGF23 as a potential prognostic marker of overall and cardiac-related mortality. In contrast, systemic Klotho levels were reduced in patients with ST-segment-elevation MI but did not correlate with mortality. In cardiac tissue, ischemic injury significantly upregulated FGF23 expression. Although Klotho prevented FGF23-induced proteomic alterations, it did not inhibit cardiac FGF23 overexpression in the post-MI model. FGF23 represents a promising biomarker for mortality and cardiac dysfunction in patients with MI. Although Klotho does not appear to be a reliable predictor of mortality after MI, its cardioprotective properties suggest a role in modulating FGF23-driven metabolic, structural, and proliferative processes in the myocardium. J Am Heart Assoc. 2026 Feb 17;15(4):e045175. JOURNAL OF THE AMERICAN HEART ASSOCIATION 41676927 https://hdl.handle.net/20.500.12105/27592 FGF23 Klotho ischemic heart disease mortality myocardial infarction Fibroblast Growth Factor 23 as a Prognostic Biomarker in Post-Myocardial Infarction Outcomes: Influence of Renal Function and Its Modulation by Klotho.