Effective tissue repair after myocardial infarction entails a vigorous angiogenic response, guided by incompletely defined immune cell–endothelial cell interactions. We identify the monocyte- and macrophage-derived cytokine METRNL (meteorin-like) as a driver of postinfarction angiogenesis and high-affinity ligand for the stem cell factor receptor KIT (KIT receptor tyrosine kinase). METRNL mediated angiogenic effects in cultured human endothelial cells through KIT-dependent signaling pathways. In a mouse model of myocardial infarction, METRNL promoted infarct repair by selectively expanding the KIT-expressing endothelial cell population in the infarct border zone. Metrnl -deficient mice failed to mount this KIT-dependent angiogenic response and developed severe postinfarction heart failure. Our data establish METRNL as a KIT receptor ligand in the context of ischemic tissue repair.

中文翻译：

---

镍纹蛋白样通过内皮 KIT 受体酪氨酸激酶促进心脏修复

心肌梗塞后有效的组织修复需要在不完全确定的免疫细胞-内皮细胞相互作用的指导下产生强烈的血管生成反应。我们确定单核细胞和巨噬细胞衍生的细胞因子 METRNL（镍纹蛋白样）是梗死后血管生成的驱动因素，也是干细胞因子受体 KIT（KIT 受体酪氨酸激酶）的高亲和力配体。METRNL 通过 KIT 依赖性信号通路介导培养的人内皮细胞的血管生成作用。在小鼠心肌梗塞模型中，METRNL 通过选择性扩大梗塞边界区表达 KIT 的内皮细胞群来促进梗塞修复。梅特尔-缺陷小鼠未能产生这种依赖于 KIT 的血管生成反应，并出现严重的梗塞后心力衰竭。我们的数据表明 METRNL 作为缺血组织修复中的 KIT 受体配体。