Myocardial infarction (MI) is a leading cause of death worldwide and requires development of efficient therapeutic strategies . Mesenchymal stem cells (MSCs) -based therapy of MI has been promising but inefficient due to undesirable microenvironment of the infarct tissue. Hence, the current study was conducted to fortify MSCs against the unfavorable microenvironment of infarct tissue via overexpression of Lipocalin 2 (Lcn2) as a cytoprotective factor. The engineered cells (Lcn2-MSCs) were transplanted to infarcted heart of a rat model of MI. According to our findings, Lcn2 overexpression resulted in increased MSCs survival in the MI tissue (p < 0.05) compared to non-engineered cells. Furthermore, the infusion of Lcn2-MSCs mitigated Left ventricle (LV) remodeling, decreased fibrosis (p < 0.0001), and reduced apoptotic death of the LVs’ cells (p < 0.0001) compared to the control. Our findings suggest a potential novel therapeutic strategy for MI, however, further investigations such as safety and efficacy assessments in large animals followed by clinical trials are required.

中文翻译：

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脐血来源的间充质干细胞过表达Lipocalin 2的移植可改善大鼠急性心肌梗死模型中的缺血性损伤并减少细胞死亡。

心肌梗塞（MI）是全球范围内的主要死亡原因，需要开发有效的治疗策略。基于心肌的间充质干细胞（MSCs）的治疗是有希望的，但是由于梗塞组织的不良微环境，其效率低下。因此，进行了当前的研究，以通过过度表达作为细胞保护因子的Lipocalin 2（Lcn2）来增强MSC抵抗梗塞组织的不利微环境。将工程细胞（Lcn2-MSC）移植到MI大鼠模型的梗塞心脏。根据我们的发现， 与未工程化的细胞相比，Lcn2的过表达导致MI组织中MSC的存活增加（p <0.05）。此外，输注Lcn2-MSC减轻左心室（LV）重塑，减少纤维化（p <0.0001），并且与对照组相比，LVs细胞的凋亡死亡减少（p <0.0001）。我们的发现表明，MI可能是一种新颖的治疗策略，但是，还需要进一步的研究，例如大型动物的安全性和功效评估，然后进行临床试验。