Journal
EXPERIMENTAL AND MOLECULAR MEDICINE
Volume 47, Issue -, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/emm.2014.122
Keywords
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Funding
- NRF [2012R1A2A1A01002881]
- Protein Metabolism Medical Research Center through Seoul National University Nobel Laureates Invitation program
- National Research Foundation of Korea [2012R1A2A1A01002881, 2013H1A2A1033261] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Many researchers have reported that oxidative damage to mitochondrial DNA (mtDNA) is increased in several age-related disorders. Damage to mitochondrial constituents and mtDNA can generate additional mitochondrial dysfunction that may result in greater reactive oxygen species production, triggering a circular chain of events. However, the mechanisms underlying this vicious cycle have yet to be fully investigated. In this review, we summarize the relationship of oxidative stress-induced mitochondrial dysfunction with mtDNA mutation in neurodegenerative disorders.
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