德国汉诺威医学院Kai C. Wollert研究组发现METRNL（meteorin-like）通过内皮 KIT 受体酪氨酸激酶促进心脏修复。相关论文发表在2022年6月17日出版的《科学》杂志上。

他们将单核细胞和巨噬细胞来源的细胞因子 METRNL鉴定为梗死后血管生成的驱动因子和干细胞因子受体 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中的血管生成作用。在心肌梗塞的小鼠模型中，METRNL 通过选择性地扩大梗塞边界区域中表达 KIT 的内皮细胞群来促进梗塞修复。Metrnl 缺陷小鼠未能产生这种依赖于 KIT 的血管生成反应，并发展为严重的梗死后心力衰竭。他们的数据将 METRNL 确立为缺血组织修复背景下的 KIT 受体配体。

研究人员表示，心肌梗死后有效的组织修复需要在不完全定义的免疫细胞-内皮细胞相互作用的指导下，产生强烈的血管生成反应。

附：英文原文

Title: Meteorin-like promotes heart repair through endothelial KIT receptor tyrosine kinase

Author: Marc R. Reboll, Stefanie Klede, Manuel H. Taft, Chen-Leng Cai, Loren J. Field, Kory J. Lavine, Andrew L. Koenig, Jenni Fleischauer, Johann Meyer, Axel Schambach, Hans W. Niessen, Maike Kosanke, Joop van den Heuvel, Andreas Pich, Johann Bauersachs, Xuekun Wu, Linqun Zheng, Yong Wang, Mortimer Korf-Klingebiel, Felix Polten, Kai C. Wollert

Issue&Volume: 2022-06-17

Abstract: 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.

DOI: abn3027

Source: https://www.science.org/doi/10.1126/science.abn3027