Cardiac FGF23: new insights into the role and function of FGF23 after acute myocardial infarction.

摘要: Abstract Objective We aimed to elucidate the local role of FGF23 after myocardial infarction in a mouse model induced by left anterior descending artery (LAD) ligation. Approach and results (C57BL/6 N) mice underwent MI via LAD ligation were sacrificed at different time-points post MI. The expression influence on fibroblast macrophages was also analyzed using isolated murine cells. identified enhanced cardiac mRNA time-dependent manner with an early increase, already first day protein abundantly detected infarcted area during inflammatory phase. While described be primarily produced bone or macrophages, we fibroblasts as only source production Inflammatory mediators, such IL-1β, IL-6 TNF-α, able induce these fibroblasts. Interestingly, not detect later time points mature scar tissue remote myocardium, most likely due TGF-β1, which have shown inhibit FGF23. FGFR1c abundant receptor for myocardium increased migration fibroblast, well Collagen 1, Periostin, Fibronectin MMP8. TGF-β1 M2 polarized macrophages. Conclusion In conclusion, produce express its respective receptors manner, thus potentially influencing resident cell migration. transitory towards complex ischemia warrants further exploration, considering ventricular remodeling.