Lam Yuen Ting
The Heart Research Institute, 7 Eliza Street, Newtown, Sydney, NSW 2042, Australia.
Oxid Med Cell Longev. 2015;2015:7095901. doi: 10.1155/2016/7095901. Epub 2015 Nov 30.
Reactive oxygen species (ROS) regulate bone marrow microenvironment for stem and progenitor cells functions including self-renewal, differentiation, and cell senescence. In response to ischemia, ROS also play a critical role in mediating the mobilization of endothelial progenitor cells (EPCs) from the bone marrow to the sites of ischemic injury, which contributes to postnatal neovascularization. Aging is an unavoidable biological deteriorative process with a progressive decline in physiological functions. It is associated with increased oxidative stress and impaired ischemia-induced neovascularization. This review discusses the roles of ROS in regulating stem and progenitor cell function, highlighting the impact of unbalanced ROS levels on EPC dysfunction and the association with age-related impairment in ischemia-induced neovascularization. Furthermore, it discusses strategies that modulate the oxidative levels of stem and progenitor cells to enhance the therapeutic potential for elderly patients with cardiovascular disease.
活性氧(ROS)调节骨髓微环境,以维持干细胞和祖细胞的功能,包括自我更新、分化和细胞衰老。在缺血反应中,ROS在介导内皮祖细胞(EPCs)从骨髓向缺血损伤部位的动员过程中也发挥着关键作用,这有助于出生后的血管新生。衰老是一个不可避免的生物退化过程,生理功能会逐渐下降。它与氧化应激增加和缺血诱导的血管新生受损有关。本综述讨论了ROS在调节干细胞和祖细胞功能中的作用,强调了ROS水平失衡对EPC功能障碍的影响以及与缺血诱导的血管新生中与年龄相关损伤的关联。此外,还讨论了调节干细胞和祖细胞氧化水平以增强老年心血管疾病患者治疗潜力的策略。