线粒体
生物
线粒体融合
氧化磷酸化
DNAJA3公司
线粒体DNA
疾病
粒线体疾病
活性氧
细胞凋亡
氧化损伤
遗传学
氧化应激
细胞生物学
基因
医学
病理
生物化学
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:1999-03-05
卷期号:283 (5407): 1482-1488
被引量:2856
标识
DOI:10.1126/science.283.5407.1482
摘要
Over the past 10 years, mitochondrial defects have been implicated in a wide variety of degenerative diseases, aging, and cancer. Studies on patients with these diseases have revealed much about the complexities of mitochondrial genetics, which involves an interplay between mutations in the mitochondrial and nuclear genomes. However, the pathophysiology of mitochondrial diseases has remained perplexing. The essential role of mitochondrial oxidative phosphorylation in cellular energy production, the generation of reactive oxygen species, and the initiation of apoptosis has suggested a number of novel mechanisms for mitochondrial pathology. The importance and interrelationship of these functions are now being studied in mouse models of mitochondrial disease.
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