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PPAR Research
Volume 2012, Article ID 348245, 12 pages
Review Article

Transcriptional Regulation by Nuclear Corepressors and PGC-1α: Implications for Mitochondrial Quality Control and Insulin Sensitivity

1Key Laboratory of Adolescent Health Assessment and Exercise Intervention, East China Normal University, Shanghai 200241, China
2College of Physical Education and Health, East China Normal University, Shanghai 200241, China

Received 10 September 2012; Revised 6 November 2012; Accepted 13 November 2012

Academic Editor: Tetsuo Yamaguchi

Copyright © 2012 Zhengtang Qi and Shuzhe Ding. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The peroxisome proliferator-activated receptors (PPARs) and estrogen-related receptor (ERRα) are ligand-activated nuclear receptors that coordinately regulate gene expression. Recent evidence suggests that nuclear corepressors, NCoR, RIP140, and SMRT, repress nuclear receptors-mediated transcriptional activity on specific promoters, and thus regulate insulin sensitivity, adipogenesis, mitochondrial number, and activity in vivo. Moreover, the coactivator PGC-1α that increases mitochondrial biogenesis during exercise and calorie restriction directly regulates autophagy in skeletal muscle and mitophagy in the pathogenesis of Parkinson's disease. In this paper, we discuss the PGC-1α’s novel role in mitochondrial quality control and the role of nuclear corepressors in regulating insulin sensitivity and interacting with PGC-1α.