期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 17, 期 12, 页码 -出版社
MDPI
DOI: 10.3390/ijms17122078
关键词
oxidative stress; hypoxic-ischemic encephalopathy; cell damage; therapeutic strategy
资金
- Major International (Regional) Joint Research Project [2008DFA31140, 2010DFA32660]
- Chinese Science and Technology Support Program [2011BAI11B22]
- National Natural Sciences Foundation of China [81370230, 81500231, 81570279]
- United Bank of Switzerland-Optimus Foundation [6102]
- Natural Sciences Foundation of Hunan Province [2016JJ6118]
- Natural Sciences Foundation of Guangdong Province [S2013010014009]
- Key Discipline Construction Fund Grant from the Third Xiangya Hospital of Central South University
- New Xiangya Talent Project from the Third Xiangya Hospital of Central South University [JJ201524]
- Technology Foundation for Selected Overseas Chinese Scholar
- Ministry of Human Resources and Social Security of China
- Ministry of Education, Culture, Sports, Science and Technology of Japan [15F15756, 15K10043]
- Grants-in-Aid for Scientific Research [15F15756] Funding Source: KAKEN
Hypoxic-ischemic encephalopathy (HIE) is one of the leading causes of morbidity and mortality in neonates. Because of high concentrations of sensitive immature cells, metal-catalyzed free radicals, non-saturated fatty acids, and low concentrations of antioxidant enzymes, the brain requires high levels of oxygen supply and is, thus, extremely sensitive to hypoxia. Strong evidence indicates that oxidative stress plays an important role in pathogenesis and progression. Following hypoxia and ischemia, reactive oxygen species (ROS) production rapidly increases and overwhelms antioxidant defenses. A large excess of ROS will directly modify or degenerate cellular macromolecules, such as membranes, proteins, lipids, and DNA, and lead to a cascading inflammatory response, and protease secretion. These derivatives are involved in a complex interplay of multiple pathways (e.g., inflammation, apoptosis, autophagy, and necrosis) which finally lead to brain injury. In this review, we highlight the molecular mechanism for oxidative stress in HIE, summarize current research on therapeutic strategies utilized in combating oxidative stress, and try to explore novel potential clinical approaches.
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