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Cited by 379

The DOI matches its Crossref record; 217 of the 217 references it cites were found in a registry or an index.

PPARα: Energy Combustion, Hypolipidemia, Inflammation and Cancer

Open access
Pyper, Sean R., Viswakarma, Navin, Yu, Songtao, Reddy, Janardan K.·2010·Nuclear Receptor Signaling

Abstract

The peroxisome proliferator-activated receptor α (PPARα, or NR1C1) is a nuclear hormone receptor activated by a structurally diverse array of synthetic chemicals known as peroxisome proliferators. Endogenous activation of PPARα in liver has also been observed in certain gene knockout mouse models of lipid metabolism, implying the existence of enzymes that either generate (synthesize) or degrade endogenous PPARα agonists. For example, substrates involved in fatty acid oxidation can function as PPARα ligands. PPARα serves as a xenobiotic and lipid sensor to regulate energy combustion, hepatic steatosis, lipoprotein synthesis, inflammation and liver cancer. Mainly, PPARα modulates the activities of all three fatty acid oxidation systems, namely mitochondrial and peroxisomal β-oxidation and microsomal co-oxidation, and thus plays a key role in energy expenditure. Sustained activation of PPARα by either exogenous or endogenous agonists leads to the development of hepatocellular carcinoma resulting from sustained oxidative and possibly endoplasmic reticulum stress and liver cell proliferation. PPARα requires transcription coactivator PPAR-binding protein (PBP)/mediator subunit 1(MED1) for its transcriptional activity.

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Metadata

Authors
Pyper, S. R., Viswakarma, N., Yu, S., & Reddy, J. K.
Venue
Nuclear Receptor Signaling
Published
2010-01
Volume
8
Issue
1
Pages
e002-e002
ISSN
1550-7629 (ISSN-L)
OpenAlex
W1974658675
Cited by
379
References
217
FWCI
14.30
Type
journal article
Language
en
Open access
hybrid

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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