Potential Signal Pathways and Therapeutic Effects of Mesenchymal Stem Cell on Oxidative Stress in Diseases.

IF 2.6 4区 医学 Q2 PHARMACOLOGY & PHARMACY Current pharmaceutical design Pub Date : 2024-09-10 DOI:10.2174/0113816128308454240823074555
Yina Xie, Lingqian Zheng, Wenmin Chen, Yang Zeng, Kaijin Yao, Tianbiao Zhou
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Abstract

Oxidative stress is a biological stress response produced by the destruction of redox equilibrium in aerobic metabolism in organisms, which is closely related to the occurrence of many diseases. Mesenchymal stem cells (MSCs) have been found to improve oxidative stress injury in a variety of diseases, including arthritis, chronic obstructive pulmonary disease, asthma, multiple sclerosis, focal segmental glomerulosclerosis, diabetic nephropathy, ischemia-reperfusion injury, hepatic fibrosis, myocardial infarction, diabetes, inflammatory bowel disease, etc. The antioxidant stress capacity of MSCs may be a breakthrough in the treatment of these diseases. This review found that MSCs have the ability to resist oxidative stress, which may be achieved through MSCs involvement in mediating the Nrf2, MAPK, NF-κB, AMPK, PI3K/AKT and Wnt/b-catenin signaling pathways.

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间充质干细胞对疾病中氧化应激的潜在信号通路和治疗效果。
氧化应激是生物体有氧代谢中氧化还原平衡遭到破坏而产生的一种生物应激反应,与多种疾病的发生密切相关。研究发现,间充质干细胞(MSCs)可改善多种疾病的氧化应激损伤,包括关节炎、慢性阻塞性肺病、哮喘、多发性硬化、局灶节段性肾小球硬化、糖尿病肾病、缺血再灌注损伤、肝纤维化、心肌梗死、糖尿病、炎症性肠病等。间充质干细胞的抗氧化应激能力可能是治疗这些疾病的突破口。本综述发现,间充质干细胞具有抗氧化能力,这可能是通过间充质干细胞参与介导Nrf2、MAPK、NF-κB、AMPK、PI3K/AKT和Wnt/b-catenin信号通路实现的。
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来源期刊
CiteScore
6.30
自引率
0.00%
发文量
302
审稿时长
2 months
期刊介绍: Current Pharmaceutical Design publishes timely in-depth reviews and research articles from leading pharmaceutical researchers in the field, covering all aspects of current research in rational drug design. Each issue is devoted to a single major therapeutic area guest edited by an acknowledged authority in the field. Each thematic issue of Current Pharmaceutical Design covers all subject areas of major importance to modern drug design including: medicinal chemistry, pharmacology, drug targets and disease mechanism.
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