期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 16, 期 12, 页码 1476-1491出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2011.4259
关键词
-
Significance: Detailed knowledge about cell death and cell survival mechanisms and how these pathways are impaired in neurodegenerative disorders and cancer forms the basis for future drug development for these diseases that affect millions of people around the world. Recent Advances: In neurodegenerative disorders such as Alzheimer's disease (AD), cell death pathways are inappropriately activated, resulting in neuronal cell death. In contrast, cancer cells develop resistance to apoptosis by regulating anti-apoptotic proteins signaling via mitochondria. Mounting evidence shows that mitochondrial function is central in both cancer and AD. Cancer cells typically shut down oxidative phosphorylation (OXPHOS) in mitochondria and switch to glycolysis for ATP production, making them resistant to hypoxia. In AD, for example, amyloid-beta peptide (A beta) and reactive oxygen species impair mitochondrial function. Neurons therefore also switch to glycolysis to maintain ATP production and to produce molecules involved in antioxidant metabolism in an attempt to survive. Critical Issues: One critical difference between cancer cells and neurons is that cancer cells can survive without OXPHOS, while neurons are dependent on OXPHOS for long-term survival. Future Directions: This review will focus on these abnormalities of mitochondrial function shared in AD and cancer and discuss the potential mechanisms underlying links that may be key steps in the development of therapeutic strategies. Antioxid. Redox Signal. 16, 1476-1491.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据