衰老
氧化应激
线粒体
细胞生物学
活性氧
生物
内质网
程序性细胞死亡
DNA损伤
β淀粉样蛋白
血红素
炎症
生物化学
细胞凋亡
免疫学
肽
酶
DNA
作者
Nicole Yu,Mazhar Pasha,John Jia En Chua
出处
期刊:Redox biology
[Elsevier]
日期:2024-04-01
卷期号:70: 103048-103048
标识
DOI:10.1016/j.redox.2024.103048
摘要
The redox process and cellular senescence are involved in a range of essential physiological functions. However, they are also implicated in pathological processes underlying age-related neurodegenerative disorders, including Alzheimer's disease (AD). Elevated levels of reactive oxygen species (ROS) are generated as a result of abnormal accumulation of beta-amyloid peptide (Aβ), tau protein, and heme dyshomeostasis and is further aggravated by mitochondria dysfunction and endoplasmic reticulum (ER) stress. Excessive ROS damages vital cellular components such as proteins, DNA and lipids. Such damage eventually leads to impaired neuronal function and cell death. Heightened oxidative stress can also induce cellular senescence via activation of the senescence-associated secretory phenotype to further exacerbate inflammation and tissue dysfunction. In this review, we focus on how changes in the redox system and cellular senescence contribute to AD and how they are affected by perturbations in heme metabolism and mitochondrial function. While potential therapeutic strategies targeting such changes have received some attention, more research is necessary to bring them into clinical application.
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