MtDNA mutations, functional decline and turnover of mitochondria in aging

Cheng Yoong Pang, Yi Shing Ma, Yau Huei Wei*

*此作品的通信作者

研究成果: 期刊稿件文獻綜述同行評審

30 引文 斯高帕斯(Scopus)

摘要

Aging is a complex biological process that involves gradual function deterioration in various tissues and organs of an individual. Mitochondrial function decline can lead to cellular overproduction of reactive oxygen species (ROS) and increase in oxidative damage to biological molecules in the aging process. We have hypothesized that increased production of ROS by the mitochondria in affected tissues in patients with mitochondrial diseases and elderly subject results in increased oxidative stress and oxidative damage. Due to the similarity of human aging process to diseases related to bioenergetic function decline and mitochondrial DNA (mtDNA) alterations, aging is sometimes viewed as a "chronic" version of such diseases. Recent studies have also established that the expression profiles of several clusters of genes are altered, oxidative modification of proteins are increased and their turnover are decreased in tissues of old human subjects and animals. Accumulating evidence has suggested that mtDNA mutations, oxidative stress, defective disposal of dysfunctional proteins and a slower turnover of mitochondria are associated with aging.

原文英語
頁(從 - 到)3661-3675
頁數15
期刊Frontiers in Bioscience - Landmark
13
發行號10
DOIs
出版狀態已出版 - 2008
對外發佈

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