Format

Send to

Choose Destination
Curr Opin Cell Biol. 2015 Apr;33:49-54. doi: 10.1016/j.ceb.2014.11.002. Epub 2014 Dec 6.

PPARs and ERRs: molecular mediators of mitochondrial metabolism.

Author information

1
Gene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
2
Gene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA; Howard Hughes Medical Institute, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA. Electronic address: evans@salk.edu.

Abstract

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 PGC1α 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 PGC1α 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.

PMID:
25486445
PMCID:
PMC4380823
DOI:
10.1016/j.ceb.2014.11.002
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center