Members of the vascular endothelial growth factor (VEGF) family, a subfamily of the platelet‐derived growth factor family of cystine‐knot growth factors, act as signaling proteins that control both the de novo formation of the vasculature during development (vasculogenesis) and the growth of blood vessels from pre‐existing vasculature (angiogenesis). Successful wound healing or recovery from tissue ischemia requires the formation of new blood vessels to restore blood flow and supply the oxygen and nutrients required to support the growth and function of reparative cells.1 VEGF family members represent crucial regulators of this process by promoting the proliferation, migration, differentiation, and survival of endothelial cells from arteries, veins, and lymphatics. The family members, VEGF‐A, B, C, D, and placental growth factor, function by binding and activating specific tyrosine kinase receptors (VEGFR‐1, ‐2, and ‐3) to control the above‐mentioned processes. Interestingly, multiple studies have established that transplanted mesenchymal stem cells (MSCs) produce and secrete VEGF‐A to promote wound healing and recovery from hind limb ischemia by inducing angiogenesis in vivo2, 3; but do the other family members also play a role? In our first Featured Article published this month in STEM CELLS Translational Medicine, Zhu et al report that MSCs pretreated with inflammatory cytokines display enhanced angiogenic and wound‐healing capacities thanks to the expression of a specific VEGF family member protein.4 In a Related Article published recently in STEM CELLS, Yang et al described how the product of a short open reading frame within the 5′‐terminal noncoding area of Hdac7 mRNA in VEGF‐treated vascular progenitor cells induced vascular repair and angiogenesis in ischemic tissue.5

Myocardial infarction occurs when the blood flow, and hence oxygen supply, to part of the heart decreases or stops, leading to the permanent loss of cardiomyocytes, the formation of scar tissue, and the seemingly irreversible loss of cardiac function that can induce heart failure. Stem cell therapy aims to support cardiac homeostasis and the regeneration of lost cells/tissues in the adult heart through, in part, the provision of multiple growth factors and immune‐modulatory cytokines. Recent studies have provided yet more evidence that the transplantation of MSCs can support the repair of damaged cardiac tissue after myocardial infarction,6-8 with some preclinical investigations supporting the concept that MSCs derived from the heart itself, which are more oriented toward a cardiovascular phenotype, may favor better outcomes.9 Unfortunately, poor homing, low survival, and a lack of efficient engraftment in the hostile microenvironment of the injured heart represent significant obstacles to the overall efficacy of MSC therapy. However, the administration of MSCs overexpressing or pretreated with growth factors to improve therapeutic output and the implementation of enhanced MSC‐targeting strategies to improve homing may lead to significantly better outcomes. In our second Featured Article published this month in STEM CELLS Translational Medicine, Zhao et al report how the treatment of cardiac MSCs with growth differentiation factor 11 (GDF11) prompted improved cell survival, retention, and their overall therapeutic efficacy following their transplantation into the infarcted mouse heart.10 In a Related Article published recently in STEM CELLS, Chen et al described how cells engineered to target fibrin may represent an exciting means to improve MSC homing to the infarcted heart and induce greater therapeutic efficacy.11

血管内皮生长因子（VEGF）家族的成员，是胱氨酸结生长因子的血小板衍生生长因子家族的一个亚家族，可作为信号蛋白，既控制发育过程中新生血管的形成（血管生成），又控制血管新生。现有血管系统的血管生长（血管生成）。成功的伤口愈合或组织缺血恢复需要形成新的血管来恢复血流并提供支持修复细胞生长和功能所需的氧气和营养。1个VEGF家族成员通过促进血管，静脉和淋巴管内皮细胞的增殖，迁移，分化和存活，代表了这一过程的关键调节因子。家族成员VEGF-A，B，C，D和胎盘生长因子通过结合并激活特定的酪氨酸激酶受体（VEGFR-1，-2和-3）来控制上述过程而发挥作用。有趣的是，多项研究已经证实，移植的间充质干细胞（MSC）可以通过诱导体内血管生成2和3来产生并分泌VEGF-A，从而促进伤口愈合和从后肢缺血恢复。但是其他家庭成员也有作用吗？在本月发表于《STEM细胞转化医学》上的第一篇精选文章中，Zhu等人报告说，由于特定的VEGF家族成员蛋白的表达，用炎症细胞因子预处理的MSC显示出增强的血管生成和伤口愈合能力。4在最近发表于STEM CELLS的相关文章中，Yang等人描述了在VEGF处理的血管祖细胞中Hdac7 mRNA 5'末端非编码区域内的短开放阅读框的产物如何诱导缺血组织的血管修复和血管生成。5

心肌梗塞发生在心脏部分的血流量减少，从而使氧气供应减少或停止时，导致心肌细胞的永久性丧失，疤痕组织的形成以及似乎导致心脏衰竭的不可逆转的心脏功能丧失。干细胞疗法旨在通过部分提供多种生长因子和免疫调节细胞因子来支持心脏稳态和成年心脏中丢失的细胞/组织的再生。最近的研究提供了更多证据，证明MSC的移植可以支持心肌梗死后受损心脏组织的修复，[ 6-8]一些临床前研究支持这样的概念，即来自心脏本身的MSC更倾向于心血管表型，可能有利于改善预后。9不幸的是，归巢不良，存活率低和受伤心脏的敌对微环境缺乏有效的植入，是MSC治疗总体疗效的重大障碍。但是，过度表达或用生长因子预处理的MSC的给药可改善治疗效果，并实施增强的MSC靶向策略以改善归巢可能导致明显更好的结果。在本月发表于《STEM细胞转化医学》上的第二篇精选文章中，Zhao等人报道了用生长分化因子11（GDF11）治疗心脏MSC后如何将其移植到梗塞的小鼠心脏后提高了细胞存活率，保留率和整体治疗效果。10 Chen等人最近在STEM CELLS上发表的相关文章中描述了工程化针对纤维蛋白的细胞如何代表一种令人兴奋的手段，可以改善MSC归巢到梗塞心脏并诱导更大的治疗功效。11