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移植间充质干细胞对抗氧化应激的抗死亡策略。

Anti-death strategies against oxidative stress in grafted mesenchymal stem cells.

机构信息

Department of Biology Education, Pusan National University, Busan, Republic of Korea.

出版信息

Histol Histopathol. 2013 Dec;28(12):1529-36. doi: 10.14670/HH-28.1529. Epub 2013 Jun 13.

Abstract

Mesenchymal stem cells (MSCs) possess the potential for use in cell-based therapy for repair of myocardial injury. The therapeutic potential of MSCs is based on the capacity of MSCs to differentiate into cardiac tissue and release paracrine factors. However, a major problem in the clinical application of MSC-based therapy is the poor viability of transplanted MSCs at the site of graft due to harsh microenvironment conditions, such as ischemia and/or anoikis. Ischemia after myocardial infarction (MI) and interaction of MSCs with their niche is associated with increased production of reactive oxygen species (ROS). ROS hinder cell adhesion and induce detachment of cells, which induces anoikis signals in implanted MSCs. Therefore, strategies to regulate oxidative stress following the implantation of MSCs are therapeutically attractive. In this review, we first describe ROS as a major obstacle in MSC-based therapy and focus on manipulation of implanted MSCs to reduce ROS-mediated anoikis.

摘要

间充质干细胞 (MSCs) 具有用于基于细胞的心肌损伤修复的治疗潜力。MSCs 的治疗潜力基于 MSCs 分化为心脏组织和释放旁分泌因子的能力。然而,基于 MSC 的治疗的临床应用中的一个主要问题是由于恶劣的微环境条件(如缺血和/或失巢凋亡),移植的 MSC 在移植物部位的存活率低。心肌梗死后的缺血(MI)和 MSCs 与它们的龛位的相互作用与活性氧(ROS)的产生增加有关。ROS 阻碍细胞黏附并诱导细胞脱落,这会在植入的 MSC 中诱导失巢凋亡信号。因此,调节 MSC 植入后氧化应激的策略具有治疗吸引力。在这篇综述中,我们首先将 ROS 描述为 MSC 治疗的主要障碍,并重点介绍了操纵植入的 MSC 以减少 ROS 介导的失巢凋亡的方法。

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