TFAM公司
NFAT公司
肌肉肥大
转录因子
心肌细胞
细胞生物学
生物
线粒体
内科学
内分泌学
线粒体生物发生
癌症研究
医学
生物化学
基因
作者
Takeo Fujino,Tomomi Ide,Masayoshi Yamaguchi,Katsutada Onitsuka,Atsushi Tanaka,Yoshiyuki Hata,Motohiro Nishida,Takako Toda,Takaaki Kanemaru,Naoyuki Kitajima,Shinya Takazaki,Hitoshi Kurose,Dongchon Kang,Kenji Sunagawa
出处
期刊:Mitochondrion
[Elsevier]
日期:2012-07-01
卷期号:12 (4): 449-458
被引量:29
标识
DOI:10.1016/j.mito.2012.06.002
摘要
The overexpression of mitochondrial transcription factor A (TFAM) attenuates the decrease in mtDNA copy number after myocardial infarction, ameliorates pathological hypertrophy, and markedly improves survival. However, non-transgenic strategy to increase mtDNA for the treatment of pathological hypertrophy remains unknown. We produced recombinant human TFAM protein (rhTFAM). rhTFAM rapidly entered into mitochondria of cultured cardiac myocytes. rhTFAM increased mtDNA and abolished the activation of nuclear factor of activated T cells (NFAT), which is well known to activate pathological hypertrophy. rhTFAM attenuated subsequent morphological hypertrophy of myocytes as well. rhTFAM would be an attractive molecule in attenuating cardiac pathological hypertrophy.
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