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Reactive Oxygen Species Superoxide Dimutases and PTEN-p53-AKT-MDM2 Signaling Loop Network in Mesenchymal Stem/Stromal Cells Regulation

机译:间充质干细胞/间质细胞调控中的活性氧超氧化物歧化酶和PTEN-p53-AKT-MDM2信号回路网络

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摘要

Mesenchymal stromal/stem cells (MSCs) are multipotent cells that can differentiate to various specialized cells, which have the potential capacity to differentiate properly and accelerate recovery in damaged sites of the body. This stem cell technology has become the fundamental element in regenerative medicine. As reactive oxygen species (ROS) have been reported to adversely influence stem cell properties, it is imperative to attenuate the extent of ROS to the promising protective approach with MSCs’ regenerative therapy. Oxidative stress also affects the culture expansion and longevity of MSCs. Therefore, there is great need to identify a method to prevent oxidative stress and replicative senescence in MSCs. Phosphatase and tensin homologue deleted on chromosome 10/Protein kinase B, PKB (PTEN/AKT) and the tumor suppressor p53 pathway have been proven to play a pivotal role in regulating cell apoptosis by regulating the oxidative stress and/or ROS quenching. In this review, we summarize the current research and our view of how PTEN/AKT and p53 with their partners transduce signals downstream, and what the implications are for MSCs’ biology.
机译:间充质基质/干细胞(MSC)是能分化为各种专门细胞的多能细胞,它们具有适当分化的潜在能力,并能加速机体受损部位的恢复。这种干细胞技术已经成为再生医学的基本要素。据报道,活性氧(ROS)会对干细胞的特性产生不利影响,因此必须通过MSC的再生疗法将ROS的程度降低至有希望的保护方法。氧化应激还影响MSC的培养扩增和寿命。因此,非常需要确定一种防止MSC中氧化应激和复制衰老的方法。事实证明,在10号染色体/蛋白激酶B,PKB(PTEN / AKT)和肿瘤抑制物p53途径上缺失的磷酸酶和张力蛋白同源物通过调节氧化应激和/或ROS猝灭在调节细胞凋亡中起着关键作用。在这篇综述中,我们总结了当前的研究以及我们对PTEN / AKT和p53及其伴侣如何在下游转导信号以及对MSC生物学的影响的看法。

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