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<p>After myocardial infarction (MI), the heart undergoes a reparative process that includes an initial acute inflammatory phase followed by a subsequent reparative phase. The transition between these phases is crucial for cardiac recovery, but the key factors remain unclear. Meteorin-like (Metrnl) promotes anti-inflammatory/reparative macrophage polarization in the myocardium, yet its role in the acute phase post-MI is unknown. We observed that macrophages infiltrating the ischemic myocardium produced elevated levels of Metrnl in both the heart and circulation 4&#xa0;days post-MI. The absence of Metrnl in <i>Metrnl⁻/⁻</i> mice altered myocardial healing and remodeling, with an increased presence of macrophages with a more pro-inflammatory phenotype. Conversely, cardiac Metrnl overexpression restored myocardial repair and promoted a shift toward a more anti-inflammatory/reparative macrophage phenotype. Mechanistically, Metrnl regulated macrophage-dependent production of Oncostatin M (Osm), a key cytokine in the early inflammatory phase post-MI that induces cardiomyocyte production of Reg3β. Reg3β, in turn, limits pro-inflammatory macrophage activation and polarization while modulating their trafficking, ultimately influencing the duration and intensity of the pro-inflammatory phase post-MI. Thus, Metrnl plays a crucial role in cardiac repair by modulating the acute phase following myocardial infarction through its regulation of macrophage populations.</p>

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Meteorin-like regulates cardiac repair via macrophage modulation following myocardial infarction

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月31日

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  • G. Ferrer-Curriu,
  • A. Blasco-Roset,
  • A. Navarro-Gascon,
  • C. Soler-Botija,
  • F. J. Godoy-Nieto,
  • M. Monguió-Tortajada,
  • R. Cereijo,
  • T. Quesada-Lopez,
  • F. Rueda,
  • S. Roura,
  • C. Gálvez-Montón,
  • F. Villarroya,
  • A. Bayés-Genís,
  • A. Planavila

摘要

After myocardial infarction (MI), the heart undergoes a reparative process that includes an initial acute inflammatory phase followed by a subsequent reparative phase. The transition between these phases is crucial for cardiac recovery, but the key factors remain unclear. Meteorin-like (Metrnl) promotes anti-inflammatory/reparative macrophage polarization in the myocardium, yet its role in the acute phase post-MI is unknown. We observed that macrophages infiltrating the ischemic myocardium produced elevated levels of Metrnl in both the heart and circulation 4 days post-MI. The absence of Metrnl in Metrnl⁻/⁻ mice altered myocardial healing and remodeling, with an increased presence of macrophages with a more pro-inflammatory phenotype. Conversely, cardiac Metrnl overexpression restored myocardial repair and promoted a shift toward a more anti-inflammatory/reparative macrophage phenotype. Mechanistically, Metrnl regulated macrophage-dependent production of Oncostatin M (Osm), a key cytokine in the early inflammatory phase post-MI that induces cardiomyocyte production of Reg3β. Reg3β, in turn, limits pro-inflammatory macrophage activation and polarization while modulating their trafficking, ultimately influencing the duration and intensity of the pro-inflammatory phase post-MI. Thus, Metrnl plays a crucial role in cardiac repair by modulating the acute phase following myocardial infarction through its regulation of macrophage populations.