PMID- 35577989
OWN - NLM
STAT- MEDLINE
DCOM- 20221025
LR  - 20221122
IS  - 1471-0080 (Electronic)
IS  - 1471-0072 (Linking)
VI  - 23
IP  - 11
DP  - 2022 Nov
TI  - Transcriptional control of energy metabolism by nuclear receptors.
PG  - 750-770
LID - 10.1038/s41580-022-00486-7 [doi]
AB  - Transcriptional regulation of catabolic pathways is a central mechanism by which 
      cells respond to physiological cues to generate the energy required for anabolic 
      pathways, transport of molecules and mechanical work. Nuclear receptors are 
      members of a superfamily of transcription factors that transduce hormonal, 
      nutrient, metabolite and redox signals into specific metabolic gene programmes, 
      and thus hold a major status as regulators of cellular energy generation. Nuclear 
      receptors also regulate the expression of genes involved in cellular processes 
      that are implicated in energy production, including mitochondrial biogenesis and 
      autophagy. Recent advances in genome-wide approaches have considerably expanded 
      the repertoire of both nuclear receptors and metabolic genes under their direct 
      transcriptional control. To fine-tune the expression of their target genes, 
      nuclear receptors must act cooperatively with other transcription factors and 
      coregulator proteins, integrate signals from key metabolic sensory systems such 
      as the AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin 
      (mTOR) complexes and synchronize their activities with the biological clock. 
      Therefore, nuclear receptors must function as more than molecular switches for 
      small lipophilic ligands - as initially ascribed - but rather must be capable of 
      orchestrating a large ensemble of input signals. Therefore, a primary role for 
      several nuclear receptors is to serve as the focal point of transcriptional hubs 
      in energy metabolism: their molecular task is to receive and transduce multiple 
      systemic and intracellular metabolic signals to maintain energy homeostasis from 
      individual cells to the whole organism.
CI  - (c) 2022. Springer Nature Limited.
FAU - Scholtes, Charlotte
AU  - Scholtes C
AUID- ORCID: 0000-0002-4982-5308
AD  - Goodman Cancer Institute, McGill University, Montreal, QC, Canada.
FAU - Giguere, Vincent
AU  - Giguere V
AUID- ORCID: 0000-0001-9567-3694
AD  - Goodman Cancer Institute, McGill University, Montreal, QC, Canada. 
      vincent.giguere@mcgill.ca.
AD  - Department of Biochemistry, Faculty of Medicine and Health Sciences, McGill 
      University, Montreal, QC, Canada. vincent.giguere@mcgill.ca.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220516
PL  - England
TA  - Nat Rev Mol Cell Biol
JT  - Nature reviews. Molecular cell biology
JID - 100962782
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - 0 (Ligands)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - 0 (Transcription Factors)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - W36ZG6FT64 (Sirolimus)
SB  - IM
MH  - *AMP-Activated Protein Kinases/metabolism
MH  - Ligands
MH  - *TOR Serine-Threonine Kinases/metabolism
MH  - Energy Metabolism/genetics
MH  - Transcription Factors/genetics/metabolism
MH  - Receptors, Cytoplasmic and Nuclear/genetics
MH  - Sirolimus
EDAT- 2022/05/17 06:00
MHDA- 2022/10/26 06:00
CRDT- 2022/05/16 23:27
PHST- 2022/04/08 00:00 [accepted]
PHST- 2022/05/17 06:00 [pubmed]
PHST- 2022/10/26 06:00 [medline]
PHST- 2022/05/16 23:27 [entrez]
AID - 10.1038/s41580-022-00486-7 [pii]
AID - 10.1038/s41580-022-00486-7 [doi]
PST - ppublish
SO  - Nat Rev Mol Cell Biol. 2022 Nov;23(11):750-770. doi: 10.1038/s41580-022-00486-7. 
      Epub 2022 May 16.