Wenz Tina
Institute for Genetics, Cluster of Excellence, Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Straße 47A, 50674 Cologne, Germany.
J Aging Res. 2011;2011:810619. doi: 10.4061/2011/810619. Epub 2011 May 5.
Aging is the most significant risk factor for a range of degenerative disease such as cardiovascular, neurodegenerative and metabolic disorders. While the cause of aging and its associated diseases is multifactorial, mitochondrial dysfunction has been implicated in the aging process and the onset and progression of age-associated disorders. Recent studies indicate that maintenance of mitochondrial function is beneficial in the prevention or delay of age-associated diseases. A central molecule seems to be the peroxisome proliferator-activated receptor γ coactivator α (PGC-1α), which is the key regulator of mitochondrial biogenesis. Besides regulating mitochondrial function, PGC-1α targets several other cellular processes and thereby influences cell fate on multiple levels. This paper discusses how mitochondrial function and PGC-1α are affected in age-associated diseases and how modulation of PGC-1α might offer a therapeutic potential for age-related pathology.
衰老是一系列退行性疾病（如心血管疾病、神经退行性疾病和代谢紊乱）的最重要风险因素。虽然衰老及其相关疾病的病因是多因素的，但线粒体功能障碍与衰老过程以及与年龄相关疾病的发生和发展有关。最近的研究表明，维持线粒体功能有助于预防或延缓与年龄相关的疾病。一个核心分子似乎是过氧化物酶体增殖物激活受体γ共激活因子α（PGC-1α），它是线粒体生物发生的关键调节因子。除了调节线粒体功能外，PGC-1α还靶向其他几个细胞过程，从而在多个层面影响细胞命运。本文讨论了在与年龄相关的疾病中线粒体功能和PGC-1α是如何受到影响的，以及PGC-1α的调节如何可能为与年龄相关的病理提供治疗潜力。
