Fibroblast Growth Factor-9 Enhances M2 Macrophage Differentiation and Attenuates Adverse Cardiac Remodeling in the Infarcted Diabetic Heart

    March 2015 in “ PLOS ONE ”
    Dinender K. Singla, Reetu D. Singla, Latifa S. Abdelli, Carley Glass
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    Studysummary This study found that FGF-9 treatment in diabetic mice improved heart function after myocardial infarction by decreasing monocyte infiltration and promoting anti-inflammatory macrophage differentiation. Our plain-language summary of this paper — not a Tressless recommendation.
    In 2015, a study was conducted on diabetic mice to investigate the effects of Fibroblast Growth Factor-9 (FGF-9) on heart function after a myocardial infarction (MI). The study, which involved 5 animals per group, found that FGF-9 treatment significantly reduced monocyte infiltration, increased M2 macrophage differentiation, and reduced adverse cardiac remodeling. It also improved cardiac function. Furthermore, FGF-9 treatment decreased the number of pro-inflammatory M1 macrophages, reduced the expression of pro-inflammatory cytokines TNF-α and IL-6, and increased the expression of IL-10, an anti-inflammatory cytokine produced by M2 macrophages. These findings suggest that FGF-9 may play a role in reprogramming monocytes to M2 macrophages, thereby reducing inflammation and potentially attenuating adverse cardiac remodeling in the infarcted diabetic heart.
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