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PPARs and ERRs: molecular mediators of mitochondrial metabolism
#MMPMID25486445
Fan W
; Evans R
Curr Opin Cell Biol
2015[Apr]; 33
(?): 49-54
PMID25486445
show ga
Since the revitalization of 'the Warburg effect', there has been great interest
in mitochondrial oxidative metabolism, not only from the cancer perspective but
also from the general biomedical science field. As the center of oxidative
metabolism, mitochondria and their metabolic activity are tightly controlled to
meet cellular energy requirements under different physiological conditions. One
such mechanism is through the inducible transcriptional co-regulators PGC1? and
NCOR1, which respond to various internal or external stimuli to modulate
mitochondrial function. However, the activity of such co-regulators depends on
their interaction with transcriptional factors that directly bind to and control
downstream target genes. The nuclear receptors PPARs and ERRs have been shown to
be key transcriptional factors in regulating mitochondrial oxidative metabolism
and executing the inducible effects of PGC1? and NCOR1. In this review, we
summarize recent gain-of-function and loss-of-function studies of PPARs and ERRs
in metabolic tissues and discuss their unique roles in regulating different
aspects of mitochondrial oxidative metabolism.
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