为了提升心肌梗塞患者的组织修复能力和心脏功能，基于骨髓来源细胞通过旁分泌途径起效的蛋白正日益成为一项核心治疗方式。

收集了来自于急性心肌梗塞患者的骨髓来源细胞分泌的蛋白之后，研究者们使用生物信息学方法分析其分秘谱。经过功能性筛选他们发现了一种由C19orf10基因（open reading frame on chromosome 19, 位于第19位染色质的开放阅读框）编码的分泌蛋白，而这种蛋白能够促进心肌细胞的存活和血管新生。研究者们还发现，骨髓来源的单核细胞和巨噬细胞能内源性产生这种蛋白并保护和修复心肌梗塞后的心脏，而且他们将此蛋白命名为髓源性生长因子（MYDGF，myeloid-derived growth factor）。

与野生型小鼠相比，Mydgf基因敲除的小鼠表现出更大的梗塞疤痕以及更严重的收缩功能紊乱。而恢复Mydfg基因表达能显着缓解紧急梗塞之后产生的梗塞疤痕和心肌的收缩功能。此项研究首次报道了髓源性生长因子的生物学功能，并可能作为一种基于功能蛋白的修复缺血组织疗法的典型范例。（生物谷Bioon.com）

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Nature Medicine doi:10.1038/nm.3778

Myeloid-derived growth factor (C19orf10) mediates cardiac repair following myocardial infarction

Mortimer Korf-Klingebiel, Marc R Reboll, Stefanie Klede, Torben Brod, Andreas Pich, Felix Polten, L Christian Napp, Johann Bauersachs, Arnold Ganser, Eva Brinkmann, Ines Reimann, Tibor Kempf, Hans W Niessen, Jacques Mizrahi, Hans-Joachim Sch?nfeld, Antonio Iglesias, Maria Bobadilla, Yong Wang & Kai C Wollert

Paracrine-acting proteins are emerging as a central mechanism by which bone marrow cell-based therapies improve tissue repair and heart function after myocardial infarction (MI). We carried out a bioinformatic secretome analysis in bone marrow cells from patients with acute MI to identify novel secreted proteins with therapeutic potential. Functional screens revealed a secreted protein encoded by an open reading frame on chromosome 19 (C19orf10) that promotes cardiac myocyte survival and angiogenesis. We show that bone marrow-derived monocytes and macrophages produce this protein endogenously to protect and repair the heart after MI, and we named it myeloid-derived growth factor (MYDGF). Whereas Mydgf-deficient mice develop larger infarct scars and more severe contractile dysfunction compared to wild-type mice, treatment with recombinant Mydgf reduces scar size and contractile dysfunction after MI. This study is the first to assign a biological function to MYDGF, and it may serve as a prototypical example for the development of protein-based therapies for ischemic tissue repair.